Risk Of Acoustic Neuroma Research Articles

Long-term Mobile Phone Use and Acoustic Neuroma Risk – Swedish Nationwide Case-Control Study

Background: There is a concern that the radiofrequency fields emitted by mobile phones could cause cancer. Epidemiological findings so far do not support an association between mobile phone use and acoustic neuroma, but the evidence concerning long term use is limited. We conducted a case-control study with the largest number of long term (?10 years) users to date. Aims: The aim was to study: the long term effects of mobile phone use on acoustic neuroma risk, the impact of the method chosen for asking about preferred side of mobile phone use, and possible differences in the detection of acoustic neuromas between users and non-users of mobile phones. Methods: A population based case-control study was conducted in Sweden from September 2002 to August 2007. Incident acoustic neuroma cases between 20 and 69 years of age were identified in collaboration with treating clinics and from the Swedish cancer register. Controls were randomly selected from the population register, matched on age, sex and residential area. The Postal questionnaires that were used to collect exposure information were completed by 451 cases (83%) and 710 controls (65%). Results: There was no significant association between acoustic neuroma and regular use of mobile phones or with long term use (?10 years). Decreased risk estimates for use on the same side as the tumor were seen together with increased estimates for use on the opposite side when preferred side at the time of diagnosis or later, was used. This difference was greatly reduced when side changes up to 10 years before diagnosis were considered. Odds ratios were generally lower when restricting the analyses to only histologically confirmed cases. Conclusions: The data does not imply that long term mobile phone use increases the risk of acoustic neuroma. Laterality specific risk estimates for acoustic neuroma are prone to bias from reversed causality and there are indications of differential detection of this tumor.

Mobile phone use and risk of brain neoplasms and other cancers: prospective study

Results from some retrospective studies suggest a possible increased risk of glioma and acoustic neuroma in users of mobile phones. The relation between mobile phone use and incidence of intracranial central nervous system (CNS) tumours and other cancers was examined in 791,710 middle-aged women in a UK prospective cohort, the Million Women Study. Cox regression models were used to estimate adjusted relative risks (RRs) and 95% confidence intervals (CIs). Women reported mobile phone use in 1999 to 2005 and again in 2009. During 7 years' follow-up, 51,680 incident invasive cancers and 1,261 incident intracranial CNS tumours occurred. Risk among ever vs never users of mobile phones was not increased for all intracranial CNS tumours (RR = 1.01, 95% CI = 0.90-1.14, P = 0.82), for specified CNS tumour types nor for cancer at 18 other specified sites. For long-term users compared with never users, there was no appreciable association for glioma (10+ years: RR = 0.78, 95% CI = 0.55-1.10, P = 0.16) or meningioma (10+ years: RR = 1.10, 95% CI = 0.66-1.84, P = 0.71). For acoustic neuroma, there was an increase in risk with long term use vs never use (10+ years: RR = 2.46, 95% CI = 1.07-5.64, P = 0.03), the risk increasing with duration of use (trend among users, P = 0.03). In this large prospective study, mobile phone use was not associated with increased incidence of glioma, meningioma or non-CNS cancers.

Allergy and brain tumors in the INTERPHONE study: pooled results from Australia, Canada, France, Israel, and New Zealand

A history of allergy has been inversely associated with several types of cancer although the evidence is not entirely consistent. We examined the association between allergy history and risk of glioma, meningioma, acoustic neuroma, and parotid gland tumors using data on a large number of cases and controls from five INTERPHONE study countries (Australia, Canada, France, Israel, New Zealand), to better understand potential sources of bias in brain tumor case-control studies and to examine associations between allergy and tumor sites where few studies exist. A total of 793 glioma, 832 meningioma, 394 acoustic neuroma, and 84 parotid gland tumor cases were analyzed with 2,520 controls recruited during 2000-2004. Conditional logistic regression models were used to obtain odds ratios (ORs) and 95 % confidence intervals (CIs) for associations between self-reported allergy and tumor risk. A significant inverse association was observed between a history of any allergy and glioma (OR = 0.73, 95 % CI 0.60-0.88), meningioma (OR = 0.77, 95 % CI 0.63-0.93), and acoustic neuroma (OR = 0.64, 95 % CI 0.49-0.83). Inverse associations were also observed with specific allergic conditions. However, inverse associations with asthma and hay fever strengthened with increasing age of allergy onset and weakened with longer time since onset. No overall association was observed for parotid gland tumors (OR = 1.21, 95 % CI 0.73-2.02). While allergy history might influence glioma, meningioma, and acoustic neuroma risk, the observed associations could be due to information or selection bias or reverse causality.

Using the Hill viewpoints from 1965 for evaluating strengths of evidence of the risk for brain tumors associated with use of mobile and cordless phones1)

Wireless phones, i.e., mobile phones and cordless phones, emit radiofrequency electromagnetic fields (RF-EMF) when used. An increased risk of brain tumors is a major concern. The International Agency for Research on Cancer (IARC) at the World Health Organization (WHO) evaluated the carcinogenic effect to humans from RF-EMF in May 2011. It was concluded that RF-EMF is a group 2B, i.e., a "possible", human carcinogen. Bradford Hill gave a presidential address at the British Royal Society of Medicine in 1965 on the association or causation that provides a helpful framework for evaluation of the brain tumor risk from RF-EMF. All nine issues on causation according to Hill were evaluated. Regarding wireless phones, only studies with long-term use were included. In addition, laboratory studies and data on the incidence of brain tumors were considered. The criteria on strength, consistency, specificity, temporality, and biologic gradient for evidence of increased risk for glioma and acoustic neuroma were fulfilled. Additional evidence came from plausibility and analogy based on laboratory studies. Regarding coherence, several studies show increasing incidence of brain tumors, especially in the most exposed area. Support for the experiment came from antioxidants that can alleviate the generation of reactive oxygen species involved in biologic effects, although a direct mechanism for brain tumor carcinogenesis has not been shown. In addition, the finding of no increased risk for brain tumors in subjects using the mobile phone only in a car with an external antenna is supportive evidence. Hill did not consider all the needed nine viewpoints to be essential requirements. Based on the Hill criteria, glioma and acoustic neuroma should be considered to be caused by RF-EMF emissions from wireless phones and regarded as carcinogenic to humans, classifying it as group 1 according to the IARC classification. Current guidelines for exposure need to be urgently revised.

Use of mobile phones and cordless phones is associated with increased risk for glioma and acoustic neuroma

The International Agency for Research on Cancer (IARC) at WHO evaluation of the carcinogenic effect of RF-EMF on humans took place during a 24–31 May 2011 meeting at Lyon in France. The Working Group consisted of 30 scientists and categorised the radiofrequency electromagnetic fields from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields (RF-EMF), as Group 2B, i.e., a ‘possible’, human carcinogen. The decision on mobile phones was based mainly on the Hardell group of studies from Sweden and the IARC Interphone study. We give an overview of current epidemiological evidence for an increased risk for brain tumours including a meta-analysis of the Hardell group and Interphone results for mobile phone use. Results for cordless phones are lacking in Interphone. The meta-analysis gave for glioma in the most exposed part of the brain, the temporal lobe, odds ratio (OR)=1.71, 95% confidence interval (CI)=1.04–2.81 in the ≥10 years (>10 years in the Hardell group) latency group. Ipsilateral mobile phone use ≥1640h in total gave OR=2.29, 95% CI=1.56–3.37. The results for meningioma were OR=1.25, 95% CI=0.31–4.98 and OR=1.35, 95% CI=0.81–2.23, respectively. Regarding acoustic neuroma ipsilateral mobile phone use in the latency group ≥10 years gave OR=1.81, 95% CI=0.73–4.45. For ipsilateral cumulative use ≥1640h OR=2.55, 95% CI=1.50–4.40 was obtained. Also use of cordless phones increased the risk for glioma and acoustic neuroma in the Hardell group studies. Survival of patients with glioma was analysed in the Hardell group studies yielding in the >10 years latency period hazard ratio (HR)=1.2, 95% CI=1.002–1.5 for use of wireless phones. This increased HR was based on results for astrocytoma WHO grade IV (glioblastoma multiforme). Decreased HR was found for low-grade astrocytoma, WHO grades I–II, which might be caused by RF-EMF exposure leading to tumour-associated symptoms and earlier detection and surgery with better prognosis. Some studies show increasing incidence of brain tumours whereas other studies do not. It is concluded that one should be careful using incidence data to dismiss results in analytical epidemiology. The IARC carcinogenic classification does not seem to have had any significant impact on governments’ perceptions of their responsibilities to protect public health from this widespread source of radiation.

Role of Tobacco Use in the Etiology of Acoustic Neuroma

Two previous studies suggest that cigarette smoking reduces acoustic neuroma risk; however, an association between use of snuff tobacco and acoustic neuroma has not been investigated previously. The authors conducted a case-control study in Sweden from 2002 to 2007, in which 451 cases and 710 population-based controls completed questionnaires. Cases and controls were matched on gender, region, and age within 5 years. The authors estimated odds ratios using conditional logistic regression analyses, adjusted for education and tobacco use (snuff use in the smoking analysis and smoking in the snuff analysis). The risk of acoustic neuroma was greatly reduced in male current smokers (odds ratio (OR) = 0.41, 95% confidence interval (CI): 0.23, 0.74) and moderately reduced in female current smokers (OR = 0.70, 95% CI: 0.40, 1.23). In contrast, current snuff use among males was not associated with risk of acoustic neuroma (OR = 0.94, 95% CI: 0.57, 1.55). The authors’ findings are consistent with previous reports of lower acoustic neuroma risk among current cigarette smokers than among never smokers. The absence of an association between snuff use and acoustic neuroma suggests that some constituent of tobacco smoke other than nicotine may confer protection against acoustic neuroma.

Acoustic neuroma risk in relation to mobile telephone use: Results of the INTERPHONE international case–control study

Background: The rapid increase in mobile telephone use has generated concern about possible health risks of radiofrequency electromagnetic fields from these devices. Methods: A case–control study of 1105 patients with newly diagnosed acoustic neuroma (vestibular schwannoma) and 2145 controls was conducted in 13 countries using a common protocol. Past mobile phone use was assessed by personal interview. In the primary analysis, exposure time was censored at one year before the reference date (date of diagnosis for cases and date of diagnosis of the matched case for controls); analyses censoring exposure at five years before the reference date were also done to allow for a possible longer latent period. Results: The odds ratio (OR) of acoustic neuroma with ever having been a regular mobile phone user was 0.85 (95% confidence interval 0.69–1.04). The OR for ≥10 years after first regular mobile phone use was 0.76 (0.52–1.11). There was no trend of increasing ORs with increasing cumulative call time or cumulative number of calls, with the lowest OR (0.48 (0.30–0.78)) observed in the 9th decile of cumulative call time. In the 10th decile (≥1640h) of cumulative call time, the OR was 1.32 (0.88–1.97); there were, however, implausible values of reported use in those with ≥1640h of accumulated mobile phone use. With censoring at 5 years before the reference date the OR for ≥10 years after first regular mobile phone use was 0.83 (0.58–1.19) and for ≥1640h of cumulative call time it was 2.79 (1.51–5.16), but again with no trend in the lower nine deciles and with the lowest OR in the 9th decile. In general, ORs were not greater in subjects who reported usual phone use on the same side of the head as their tumour than in those who reported it on the opposite side, but it was greater in those in the 10th decile of cumulative hours of use. Conclusions: There was no increase in risk of acoustic neuroma with ever regular use of a mobile phone or for users who began regular use 10 years or more before the reference date. Elevated odds ratios observed at the highest level of cumulative call time could be due to chance, reporting bias or a causal effect. As acoustic neuroma is usually a slowly growing tumour, the interval between introduction of mobile phones and occurrence of the tumour might have been too short to observe an effect, if there is one.

WHO Classification Sparks Debate Over Cell Phone Safety

F ar from settling the question of whether cell phones cause cancer, the latest pronouncement by the World Health Organization that cell phones could “possibly” be carcinogenic has left a wake of confusion and consternation. In July ’ s The Lancet Oncology , the WHO ’ s International Agency for Research on Cancer (IARC) announced that it had classifi ed radiofrequency (RF) electromagnetic fi elds — such as those that wireless phones emit — as “possibly carcinogenic to humans” based on an increased risk of glioma and acoustic neuroma. The move came barely a year after the huge Interphone study found no increased risk of cancer from more than 10 years of cell phone use. But the Interphone results, published here in the Journal ( see J. Natl. Cancer Inst. 2010; 102:13), suggested there might be some risk for people with the heaviest use. The National Cancer Institute, the American Cancer Society, and other organizations were at pains to update their online information and reassure worried consumers that the WHO action was not based on any clinically meaningful new evidence but merely on an evaluation of the existing literature. Experts repeated the familiar mantra “more research is needed,” even as newspaper headlines warned of the potential risk. Some observers missed the small print. The IARC ’ s 2B classifi cation — “possibly carcinogenic to humans” — was based only on “limited evidence of carcinogenicity.” According to IARC, that means: “A positive association has been observed between exposure to the agent and cancer for which a causal interpretation is considered . . . to be credible, but chance, bias, or confounding could not be ruled out with reasonable confi dence.” As Jonathan Samet, M.D. , overall chair of the IARC working group and chair of preventive medicine at the University of Southern California, told a press conference in Lyon, France, on May 31, the classifi cation means “there could be some risk, and therefore we need to keep a close watch for a link between cell phones and cancer risk.”

Abstract 1873: Low-dose radiation exposure and the risk of developing acoustic neuroma

Abstract Aside from the rare hereditary syndrome of Neurofibromatosis type 2 or high-dose ionizing radiation exposure, the causes of the vast majority of acoustic neuroma development remain unclear. A hospital-based case-control study was conducted to investigate the roles of exposure to commonly used diagnostic tools and phone technology that emit low dose ionizing and non-ionizing radiation in the etiology of acoustic neuroma. A total of 353 cases were recruited from a cohort of individuals who underwent Gamma Knife Radiosurgery as primary or adjuvant management of acoustic neuroma between the years 1997-2007 at the Center for Image Guided Neurosurgery, University of Pittsburgh Medical Center (UPMC). Matched by age and gender, 353 controls without brain tumor history were recruited from the Neurosurgery spine and pain clinics at UPMC. Information on demographic characteristics, medical exposure to radiation, use of cell phone, and other potential risk factors of acoustic neuroma were collected via questionnaire by trained interviewers at clinics. Conditional multivariate logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI) to assess risk of acoustic neuroma associated with low-dose radiation exposure. Adjusted for education, smoking, drinking, occupational exposure to noise, previous history of head injury, and family history of cancer, exposure to dental x-ray every 2-3 years and at least once a year was significantly associated with development of acoustic neuroma compared to individuals exposed to dental x-ray less than once every five years (OR=3.57, 95% CI = 1.54-8.23 and OR=2.31, 95% CI=1.06-5.04, respectively). History of full mouth or panorax X-ray exam (OR=1.35, 95% CI=0.76-2.41), CAT or CT scan of head or neck (OR=0.61, 95% CI=0.30-1.23), and other X-ray exam of head or neck (OR=0.77, 95% CI=0.41-1.45) were not found to be related to development of acoustic neuroma. Use of cell phones or cordless phones for more than 10 years was not significantly associated with development of acoustic neuroma (OR=1.30, 95% CI=0.53-3.20 and OR=1.20, 95% CI=0.43-3.37, respectively). We found that frequent exposure to dental X-rays may contribute the development of acoustic neuroma, although does-response effect was not found. Further epidemiologic studies are necessary to confirm the association of diagnostic dental X-rays exposure and development of acoustic neuroma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1873. doi:10.1158/1538-7445.AM2011-1873

A case-case study of mobile phone use and acoustic neuroma risk in Japan

Results of case-control studies of mobile phone use and acoustic neuroma have been inconsistent. We conducted a case-case study of mobile phone use and acoustic neuroma using a self-administered postal questionnaire. A total of 1589 cases identified in 22 hospitals throughout Japan were invited to participate, and 787 cases (51%) actually participated. Associations between laterality of mobile phone use prior to the reference dates (1 and 5 years before diagnosis) and tumor location were analyzed. The overall risk ratio was 1.08 (95% confidence interval (CI), 0.93-1.28) for regular mobile phone use until 1 year before diagnosis and 1.14 (95% CI, 0.96-1.40) for regular mobile phone use until 5 years before diagnosis. A significantly increased risk was identified for mobile phone use for >20 min/day on average, with risk ratios of 2.74 at 1 year before diagnosis, and 3.08 at 5 years before diagnosis. Cases with ipsilateral combination of tumor location and more frequently used ear were found to have tumors with smaller diameters, suggesting an effect of detection bias. Furthermore, analysis of the distribution of left and right tumors suggested an effect of tumor-side-related recall bias for recall of mobile phone use at 5 years before diagnosis. The increased risk identified for mobile phone users with average call duration >20 min/day should be interpreted with caution, taking into account the possibilities of detection and recall biases. However, we could not conclude that the increased risk was entirely explicable by these biases, leaving open the possibility that mobile phone use increased the risk of acoustic neuroma.

Occupational exposures and risk of acoustic neuroma

ObjectivesAcoustic neuroma is a benign tumour accounting for approximately 6–10% of all intracranial tumours and occurs mainly in patients aged ≥50 years. Our aim was to investigate a wide range...

Cigarette smoking and risk of acoustic neuromas and pituitary tumours in the Million Women Study

Background:The relationship between cigarette smoking and incidence of acoustic neuromas and pituitary tumours is uncertain.Methods:We examined the relation between smoking and risk of acoustic neuromas and pituitary tumours in a prospective study of 1.2 million middle-aged women in the United Kingdom.Results:Over 10.2 million person years of follow-up, 177 women were diagnosed with acoustic neuromas and 174 with pituitary tumours. Current smokers at recruitment were at significantly reduced risk of incident acoustic neuroma compared with never smokers (adjusted relative risk (RR)=0.41, 95% confidence interval (CI)=0.24–0.70, P=0.001). Past smokers did not have significantly different risk of acoustic neuroma than never smokers (RR=0.87, 95% CI=0.62–1.22, P=0.4). Smoking was not associated with incidence of pituitary tumours (RR in current vs never smokers=0.91, 95% CI=0.60–1.40, P=0.7).Conclusion:Women who smoke are at a significantly reduced risk of acoustic neuromas, but not of pituitary tumours, compared with never smokers. Acoustic neuromas are much rarer than the cancers that are increased among smokers.

Human health effects of EMFs: The cost of doing nothing

Everyone is exposed to electromagnetic fields (EMFs) from electricity (extremely low frequency, ELF), communication frequencies and wireless devices (radiofrequency, RF), as well as naturally occurring EMFs. Concern of health hazards from EMFs has increased as the use of mobile phones and other wireless devices has grown in all segments of the population, especially children. While there has been strong evidence for an association between leukemia and residential or occupational exposure to ELF EMFs for many years, the standards in existence are not sufficiently stringent to protect from an increased risk of cancer. ELF EMFs also increase risk of at least two types of neurodegenerative diseases. For RF EMFs, standards are set at levels designed to avoid tissue heating, in spite of many reports of biological effects at intensities too low to cause significant heating. Recent evidence demonstrates elevations in risk of brain cancer and acoustic neuroma only on the side of the head where individuals used their mobile phone. Individuals who begin exposure at younger ages are more vulnerable. These data indicate that the existing standards for radiofrequency exposure are not adequate. While there are many unanswered questions, the cost of doing nothing may result in an increasing number of people, many of them young, developing these diseases.

Occupation and risk of glioma, meningioma and acoustic neuroma: Results from a German case–control study (Interphone Study Group, Germany)

Background: Several epidemiological studies have investigated the association between occupation and brain tumour risk, but results have been inconclusive. We investigated the association between six occupational categories defined a priori: chemical, metal, agricultural, construction, electrical/electronic and transport, and the risk of glioma, meningioma and acoustic neuroma. Methods: In a population-based case–control study involving a total of 844 cases and 1688 controls conducted from 2000 to 2003, detailed information on life-long job histories was collected during personal interviews and used to create job calendars for each participant. Job title, job activity, job number, and the starting and ending dates of the activity were recorded for all activities with duration of at least 1 year. Reported occupational activities were coded according to the International Standard Classification of Occupations 1988 (ISCO 88). For the analyses we focused on six a priori defined occupational sectors, namely chemical, metal, agricultural, construction, electrical/electronic and transport. Multiple conditional logistic regression analysis was used to estimate odds ratios and their 95% confidence intervals. Results: Most of the observed odds ratios were close to 1.0 for ever having worked in the six occupational sectors and risk of glioma, meningioma and acoustic neuroma. Sub-group analyses according to duration of employment resulted in two elevated odds ratios with confidence intervals excluding unity. Conclusions: We did not observe an increased risk of glioma or meningioma for occupations in the agricultural, construction, transport, chemical, electrical/electronic and metal sectors. The number of ‘significant’ odds ratios is consistent with an overall ‘null-effect’.

DNA repair gene polymorphisms and risk of adult meningioma, glioma, and acoustic neuroma

Although the etiology of primary brain tumors is largely unknown, prior studies suggest that DNA repair polymorphisms may influence risk of glioma. Altered DNA repair is also likely to affect the risk of meningioma and acoustic neuroma, but these tumors have not been well studied. We estimated the risk of glioma (n = 362), meningioma (n = 134), and acoustic neuroma (n = 69) in non-Hispanic whites with respect to 36 single nucleotide polymorphisms from 26 genes involved in DNA repair in a hospital-based, case-control study conducted by the National Cancer Institute. We observed significantly increased risk of meningioma with the T variant of GLTSCR1 rs1035938 (OR(CT/TT) = 3.5; 95% confidence interval: 1.8-6.9; P(trend) .0006), which persisted after controlling for multiple comparisons (P = .019). Significantly increased meningioma risk was also observed for the minor allele variants of ERCC4 rs1800067 (P(trend) .01); MUTYH rs3219466 (P(trend) .02), and PCNA rs25406 (P(trend) .03). The NBN rs1805794 minor allele variant was associated with decreased meningioma risk (P(trend) .006). Risk of acoustic neuroma was increased for the ERCC2 rs1799793 (P(trend) .03) and ERCC5 rs17655 (P(trend) .05) variants and decreased for the PARP1 rs1136410 (P(trend) .03). Decreased glioma risk was observed with the XRCC1 rs1799782 variant (P(trend) .04). Our results suggest that common DNA repair variants may affect the risk of adult brain tumors, especially meningioma.

ELECTROMAGNETIC FIELDS: Conference, Hearing Call Up Cell Phone Use

ELECTROMAGNETIC FIELDS: Conference, Hearing Call Up Cell Phone Use

Cell phone use and acoustic neuroma: the need for standardized questionnaires and access to industry data

Background The capacity of radiofrequency from cell phones to be absorbed into the brain has prompted concerns that regular cell phone use may increase the risk of acoustic neuroma (AN) and other brain tumors. This article critically evaluates current literature on cell phone use and AN risks and proposes additional studies to clarify any possible linkage. Methods Through a PubMed search, we identified and reviewed 10 case-control studies and 1 cohort study of AN risks associated with cell phone use and a meta-analysis of long-term mobile phone use and its association with AN and other brain tumors. Results Most studies did not find association between the development of AN and cell phone use, but some studies that followed cases for 10 years or more did show an association. Among 10 case-control studies, odds ratios for AN associated with regular cell phone use ranged from 0.5 (95% confidence interval [CI], 0.2-1.0) to 4.2 (95% CI, 1.8-10). Cell phone use was not associated with increased risk for AN in the Danish cohort study, which excluded business users from their study. The meta-analysis, which included 3 case-control studies, found that subjects who used cell phones for at least 10 years had a 2.4-fold greater risk of developing ipsilateral AN. In general, retrospective studies are limited in the ability to assess cell phone exposure because of recall bias and misclassification. Conclusions The evaluation of AN risk factors is challenging due to its long latency. Some studies of longer term cell phone use have found an increased risk of ipsilateral AN. Adopting a prospective approach to acquire data on cell phone use, obtaining retrospective billing records that provide independent evaluations of exposures, and incorporating information on other key potential risk factors from questionnaires could markedly advance the capacity of studies to evaluate the impact of cell phones on AN.

Can loud noise cause acoustic neuroma? Analysis of the INTERPHONE study in France

Objectives: To investigate possible associations between risk of acoustic neuroma and exposure to loud noise in leisure and occupational settings. Methods: A case-control study was conducted in France within the...

Epidemiological evidence for an association between use of wireless phones and tumor diseases

During recent years there has been increasing public concern on potential cancer risks from microwave emissions from wireless phones. We evaluated the scientific evidence for long-term mobile phone use and the association with certain tumors in case–control studies, mostly from the Hardell group in Sweden and the Interphone study group. Regarding brain tumors the meta-analysis yielded for glioma odds ratio (OR) = 1.0, 95% confidence interval (CI) = 0.9–1.1. OR increased to 1.3, 95% CI = 1.1–1.6 with 10 year latency period, with highest risk for ipsilateral exposure (same side as the tumor localisation), OR = 1.9, 95% CI = 1.4–2.4, lower for contralateral exposure (opposite side) OR = 1.2, 95% CI = 0.9–1.7. Regarding acoustic neuroma OR = 1.0, 95% CI = 0.8–1.1 was calculated increasing to OR = 1.3, 95% CI = 0.97–1.9 with 10 year latency period. For ipsilateral exposure OR = 1.6, 95% CI = 1.1–2.4, and for contralateral exposure OR = 1.2, 95% CI = 0.8–1.9 were found. Regarding meningioma no consistent pattern of an increased risk was found. Concerning age, highest risk was found in the age group <20 years at time of first use of wireless phones in the studies from the Hardell group. For salivary gland tumors, non-Hodgkin lymphoma and testicular cancer no consistent pattern of an association with use of wireless phones was found. One study on uveal melanoma yielded for probable/certain mobile phone use OR = 4.2, 95% CI = 1.2–14.5. One study on intratemporal facial nerve tumor was not possible to evaluate due to methodological shortcomings. In summary our review yielded a consistent pattern of an increased risk for glioma and acoustic neuroma after >10 year mobile phone use. We conclude that current standard for exposure to microwaves during mobile phone use is not safe for long-term exposure and needs to be revised.

Cancer: Strong Signal for Cell Phone Effects

Cancer: Strong Signal for Cell Phone Effects