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.     

Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects

We studied the association between use of mobile and cordless phones and malignant brain tumours. Pooled analysis was performed of two case-control studies on patients with malignant brain tumours diagnosed during 1997-2003 and matched controls alive at the time of study inclusion and one case-control study on deceased patients and controls diagnosed during the same time period. Cases and controls or relatives to deceased subjects were interviewed using a structured questionnaire. Replies were obtained for 1,251 (85%) cases and 2,438 (84%) controls. The risk increased with latency period and cumulative use in hours for both mobile and cordless phones. Highest risk was found for the most common type of glioma, astrocytoma, yielding in the >10 year latency group for mobile phone use odds ratio (OR) = 2.7, 95% confidence interval (CI) = 1.9-3.7 and cordless phone use OR = 1.8, 95% CI = 1.2-2.9. In a separate analysis, these phone types were independent risk factors for glioma. The risk for astrocytoma was highest in the group with first use of a wireless phone before the age of 20; mobile phone use OR = 4.9, 95% CI = 2.2-11, cordless phone use OR = 3.9, 95% CI = 1.7-8.7. In conclusion, an increased risk was found for glioma and use of mobile or cordless phone. The risk increased with latency time and cumulative use in hours and was highest in subjects with first use before the age of 20.     

Use of wireless phones and the risk of salivary gland tumours: a case-control study

The last decades of increasing use of wireless phones, including mobile as well as cordless desktop phones, have led to concerns about the potential carcinogenic effects of radiofrequency electromagnetic fields. Among the most exposed areas of the body when the phone is used for talking are the salivary glands, mainly the parotid gland, located in front of the ear. The objective of this case-control study was to assess whether the use of wireless phones is associated with an increased risk of tumour at this site. Sixty-nine patients with salivary gland tumours (63 with a parotid gland tumour) and 262 randomly recruited controls were included. Unconditional logistic regression - adjusted for age at diagnosis, sex, year of diagnosis and socioeconomic index - was used to produce odds ratios and 95% confidence intervals. The use of wireless phones was not associated with an overall increased risk of salivary gland tumours, odds ratio 0.8, 95% confidence interval 0.4-1.5. Neither was there an increased risk for the different phone types when calculated separately nor was there an increased risk for different latencies or when cumulative use was divided into three groups (1-1000, 1001-2000 and >2000 h). The overall results were similar for the risk of parotid gland tumours. In conclusion, our data add to the evidence against there being an increased risk for parotid gland tumours associated with light-to-moderate use of wireless phones and for less than 10 years of use but offers little information on risk related to more prolonged and/or heavy use.     

Mobile phone use and risk of glioma in 5 North European countries

Public concern has been expressed about the possible adverse health effects of mobile telephones, mainly related to intracranial tumors. We conducted a population-based case-control study to investigate the relationship between mobile phone use and risk of glioma among 1,522 glioma patients and 3,301 controls. We found no evidence of increased risk of glioma related to regular mobile phone use (odds ratio, OR = 0.78, 95% confidence interval, CI: 0.68, 0.91). No significant association was found across categories with duration of use, years since first use, cumulative number of calls or cumulative hours of use. When the linear trend was examined, the OR for cumulative hours of mobile phone use was 1.006 (1.002, 1.010) per 100 hr, but no such relationship was found for the years of use or the number of calls. We found no increased risks when analogue and digital phones were analyzed separately. For more than 10 years of mobile phone use reported on the side of the head where the tumor was located, an increased OR of borderline statistical significance (OR = 1.39, 95% CI 1.01, 1.92, p trend 0.04) was found, whereas similar use on the opposite side of the head resulted in an OR of 0.98 (95% CI 0.71, 1.37). Although our results overall do not indicate an increased risk of glioma in relation to mobile phone use, the possible risk in the most heavily exposed part of the brain with long-term use needs to be explored further before firm conclusions can be drawn.     

Association between brain tumors and menopausal status.

BACKGROUND: Several lines of evidence have implicated female hormones in the etiology of human brain tumors, meningiomas in particular. PURPOSE: To investigate the relationship between brain tumor development and the hormonal changes manifested during pregnancy and menopause, we analyzed data from female participants in a population-based case-control study of adult brain tumors. This study was conducted in 1987-1988 in the Rhein-Neckar-Odenwald area of the Federal Republic of Germany. METHODS: The study population consisted of 127 women with meningiomas, gliomas, and acoustic neuromas (case patients) and 233 control women who were selected from the general population and frequency-matched by age to the case patients. Information on parity, menopausal status, and previous gynecologic surgeries was obtained through a standardized questionnaire. Case patients and control subjects were compared with the use of the unconditional maximum likelihood estimation of the parameters in a logistic regression model. RESULTS: Our results were not statistically significant; nevertheless, they revealed some interesting trends. No association was found between parity and the development of any of the three histological subtypes of brain tumor (relative risk [RR] = 1.31; 95% confidence interval [CI] = 0.51-2.07). Menopausal women had a greatly reduced risk of developing meningiomas (RR = 0.58; 95% CI = 0.18-1.90), and this effect was most pronounced when menopause had been surgically induced by bilateral oophorectomy (RR = 0.12; 95% CI = 0.01-1.30). Menopausal women had a greater risk of developing gliomas or acoustic neuromas (RR = 1.77; 95% CI = 0.67-4.68), except when menopause was surgically induced, in which case the risk was reduced (RR = 0.33; 95% CI = 0.04-3.09). Oophorectomy after menopause did not appear to influence risk. CONCLUSIONS: Since the onset of menopause is accompanied by cessation of estrogen production, our results support the notion that female hormones play a role in the development of brain tumors.     

Further aspects on cellular and cordless telephones and brain tumours

We included in a case-control study on brain tumours and mobile and cordless telephones 1,617 patients aged 20-80 years of both sexes diagnosed during January 1, 1997 to June 30, 2000. They were alive at the study time and had histopathology verified brain tumour. One matched control to each case was selected from the Swedish Population Register. The study area was the Uppsala-Orebro, Stockholm, Link?ping and G?teborg medical regions of Sweden. Exposure was assessed by a questionnaire that was answered by 1,429 (88%) cases and 1,470 (91%) controls. In total use of analogue cellular telephones gave an increased risk with odds ratio (OR)=1.3, 95% confidence interval (CI)=1.04-1.6, whereas digital and cordless phones did not overall increase the risk significantly. Ipsilateral use of analogue phones gave OR=1.7, 95% CI=1.2-2.3, digital phones OR=1.3, 95% CI=1.02-1.8 and cordless phones OR=1.2, 95% CI=0.9-1.6. The risk for ipsilateral use was significantly increased for astrocytoma for all studied phone types, analogue phones OR=1.8,95% CI=1.1-3.2, digital phones OR=1.8, 95% CI=1.1-2.8, cordless phones OR=1.8, 95% CI=1.1-2.9. Use of a telephone on the opposite side of the brain was not associated with a significantly increased risk for brain tumours. Regarding anatomical area of the tumour and exposure to microwaves, the risk was increased for tumours located in the temporal area on the same side of the brain that was used during phone calls, significantly so for analogue cellular telephones OR=2.3, 95% CI=1.2-4.1. For acoustic neurinoma OR=4.4, 95% CI=2.1-9.2 was calculated among analogue cellular telephone users. When duration of use was analysed as a continuous variable in the total material, the risk increased per year for analogue phones with OR=1.04, 95% CI=1.01-1.08. For astrocytoma and ipsilateral use the trend was for analogue phones OR=1.10, 95% CI=1.02-1.19, digital phones OR=1.11, 95% CI=1.01-1.22, and cordless phones OR=1.09, 95% CI=1.01-1.19. There was a tendency of a shorter tumour induction period for ipsilateral exposure to microwaves than for contralateral, which may indicate a tumour promotor effect.     

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.     

Environmental risk factors for sporadic acoustic neuroma (Interphone Study Group, Germany)

The only known risk factor for sporadic acoustic neuroma is high-dose ionising radiation. Environmental exposures, such as radiofrequency electromagnetic fields and noise are under discussion, as well as an association with allergic diseases. We performed a population-based case-control study in Germany investigating these risk factors in 97 cases with acoustic neuroma, aged 30 to 69 years, and in 194 matched controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated in multiple logistic regression models. Increased risks were found for exposure to persistent noise (OR=2.31; 95% CI 1.15-4.66), and for hay fever (OR=2.20; 95% CI 1.09-4.45), but not for ionising radiation (OR=0.91; 95 % CI 0.51-1.61) or regular mobile phone use (OR=0.67; 95% CI 0.38-1.19). The study confirms results of recently published studies, although the pathogenetic mechanisms are still unknown.     

Occupational and residential exposure to electromagnetic fields and risk of brain tumors in adults: a case-control study in Gironde, France

The etiology of brain tumors remains largely unknown. Among potential risk factors, exposure to electromagnetic fields is suspected. We analyzed the relationship between residential and occupational exposure to electromagnetic field and brain tumors in adults. A case-control study was carried out in southwestern France between May 1999 and April 2001. A total of 221 central nervous system tumors (105 gliomas, 67 meningiomas, 33 neurinomas and 16 others) and 442 individually age- and sex-matched controls selected from general population were included. Electromagnetic field exposure [extremely low frequency (ELF) and radiofrequency separately was assessed in occupational settings through expert judgement based on complete job calendar, and at home by assessing the distance to power lines with the help of a geographical information system. Confounders such as education, use of home pesticide, residency in a rural area and occupational exposure to chemicals were taken into account. Separate analyses were performed for gliomas, meningiomas and acoustic neurinomas. A nonsignificant increase in risk was found for occupational exposure to electromagnetic fields [odds ratio (OR = 1.52, 0.92-2.51)]. This increase became significant for meningiomas, especially when considering ELF separately [OR = 3.02; 95 percent confidence interval (95% CI) =1.10-8.25]. The risk of meningioma was also higher in subjects living in the vicinity of power lines (<100 m), even if not significant (OR = 2.99, 95% CI 0.86-10.40). These data suggest that occupational or residential exposure to ELF may play a role in the occurrence of meningioma.     

Meta-analysis of long-term mobile phone use and the association with brain tumours

We evaluated long-term use of mobile phones and the risk for brain tumours in case-control studies published so far on this issue. We identified ten studies on glioma and meta-analysis yielded OR = 0.9, 95% CI = 0.8-1.1. Latency period of > or =10-years gave OR = 1.2, 95% CI = 0.8-1.9 based on six studies, for ipsilateral use (same side as tumour) OR = 2.0, 95% CI = 1.2-3.4 (four studies), but contralateral use did not increase the risk significantly, OR = 1.1, 95% CI = 0.6-2.0. Meta-analysis of nine studies on acoustic neuroma gave OR = 0.9, 95% CI = 0.7-1.1 increasing to OR = 1.3, 95% CI = 0.6-2.8 using > or =10-years latency period (four studies). Ipsilateral use gave OR = 2.4, 95% CI = 1.1-5.3 and contra-lateral OR = 1.2, 95% CI = 0.7-2.2 in the > or =10-years latency period group (three studies). Seven studies gave results for meningioma yielding overall OR = 0.8, 95% CI = 0.7-0.99. Using > or =10-years latency period OR = 1.3, 95% CI = 0.9-1.8 was calculated (four studies) increasing to OR = 1.7, 95% CI = 0.99-3.1 for ipsilateral use and OR = 1.0, 95% CI = 0.3-3.1 for contralateral use (two studies). We conclude that this meta-analysis gave a consistent pattern of an association between mobile phone use and ipsilateral glioma and acoustic neuroma using > or =10-years latency period.     

Hormone replacement therapy and incidence of central nervous system tumours in the Million Women Study

We examined the relation between the use of hormone replacement therapy (HRT) and the incidence of central nervous system (CNS) tumours in a large prospective study of 1,147,894 postmenopausal women. Women were aged 56.6 years on average at entry, and HRT use was recorded at recruitment and updated, where possible, about 3 years later. During a mean follow‐up of 5.3 years per woman, 1,266 CNS tumours were diagnosed, including 557 gliomas, 311 meningiomas and 117 acoustic neuromas. Compared with never users of HRT, the relative risks (RRs) for all incident CNS tumours, gliomas, meningiomas and acoustic neuromas in current users of HRT were 1.20 (95% CI: 1.05–1.36), 1.09 (95% CI: 0.89–1.32), 1.34 (95% CI: 1.03–1.75) and 1.58 (95% CI: 1.02–2.45), respectively, and there was no significant difference in the relative risks by tumour type (heterogeneity p = 0.2). In past users of HRT the relative risk was 1.07 (95% CI: 0.93–1.24) for all CNS tumours. Among current users of HRT, there was significant heterogeneity by the type of HRT with the users of oestrogen‐only HRT at higher risk of all CNS tumours than users of oestrogen–progestagen HRT (RR = 1.42, 95% CI: 1.21–1.67 versus RR = 0.97, 95% CI: 0.82–1.16) (heterogeneity p < 0.001). Among current users of oestrogen‐only and oestrogen–progestagen HRT, there was no significant heterogeneity by duration of use, hormonal constituent or mode of administration of HRT.     

Sex hormone receptors in intracranial tumours and normal brain

Fifty-four intracranial neoplasms (29 meningiomas, 16 gliomas, seven acoustic neuromas and two cerebral metastases) and nine specimens of normal brain were evaluated for specific progesterone and oestrogen receptor proteins using a dextran-coated charcoal assay and Scatchard plot analysis. Sixteen meningiomas (55%) were progesterone receptor (PgR) positive (median 52; mean 120; range 10-486 fmol mg-1 cytosol protein), whilst all were oestrogen receptor negative (ER-). Two (28%) of the acoustic neuromas contained small amounts of PgR protein, but all seven were ER-. None of the gliomas, cerebral metastases or specimens of normal brain contained ER or PgR protein. Analysis of PgR status and clinicopathological data suggest that there is no predictive correlation between PgR status and the patients age, sex, reproductive status, tumour histology or tumour behaviour. These results again suggest that in meningiomas PgR proteins are not modulated by oestrogens acting through ER. This finding may explain the failure of antioestrogen therapy to influence the growth of meningiomas. The significance of PgR protein in intracranial meningiomas is discussed with respect to tumour heterogeneity and implications for research with gene probes.     

A case-control study of risk of leukaemia in relation to mobile phone use

Background:

Mobile phone use is now ubiquitous, and scientific reviews have recommended research into its relation to leukaemia risk, but no large studies have been conducted.

Methods:

In a case–control study in South East England to investigate the relation of acute and non-lymphocytic leukaemia risk to mobile phone use, 806 cases with leukaemia incident 2003–2009 at ages 18–59 years (50% of those identified as eligible) and 585 non-blood relatives as controls (provided by 392 cases) were interviewed about mobile phone use and other potentially aetiological variables.

Results:

No association was found between regular mobile phone use and risk of leukaemia (odds ratio (OR)=1.06, 95% confidence interval (CI)=0.76, 1.46). Analyses of risk in relation to years since first use, lifetime years of use, cumulative number of calls and cumulative hours of use produced no significantly raised risks, and there was no evidence of any trends. A non-significantly raised risk was found in people who first used a phone 15 or more years ago (OR=1.87, 95% CI=0.96, 3.63). Separate analyses of analogue and digital phone use and leukaemia subtype produced similar results to those overall.

Conclusion:

This study suggests that use of mobile phones does not increase leukaemia risk, although the possibility of an effect after long-term use, while biologically unlikely, remains open.     

Cimetidine and other histamine2-receptor antagonist use in relation to risk of breast cancer.

OBJECTIVE: Cimetidine, a histamine2-receptor antagonist (H2 blocker) commonly used to treat symptoms of peptic and duodenal ulcer, influences both hormonal and immune pathways. We investigated the influence of cimetidine use on the risk of breast cancer in our hospital-based case control surveillance study. METHODS: Data on medication use and other factors were elicited from patients admitted to hospitals from 1977 to 2002. We compared 6,994 breast cancer cases with a control group comprising cancer (n = 2,478) and noncancer (n = 6,004) diagnoses. Conditional logistic regression models were used to estimate odds ratios for H2 blocker use that began at least 1 year prior to admission. Regular use was defined as use for at least 4 days per week for at least 3 continuous months. RESULTS: The odds ratio for breast cancer among regular users of cimetidine was 0.9 (95% confidence interval, 0.6-1.2) using a combined cancer and noncancer control group. For use of 4 or more years' duration, the odds ratio was < 1.0 but was not statistically significant. The odds ratio for the regular use of other H2 blockers was 0.9 (95% confidence interval, 0.6-1.3). CONCLUSIONS: Our data agree with data from three prior studies which indicate that cimetidine is not associated with the risk of breast cancer. Other H2 blockers were also unrelated to the risk of breast cancer.     

Mobile phone use, exposure to radiofrequency electromagnetic field, and brain tumour: a case-control study

In a case-control study in Japan of brain tumours in relation to mobile phone use, we used a novel approach for estimating the specific absorption rate (SAR) inside the tumour, taking account of spatial relationships between tumour localisation and intracranial radiofrequency distribution. Personal interviews were carried out with 88 patients with glioma, 132 with meningioma, and 102 with pituitary adenoma (322 cases in total), and with 683 individually matched controls. All maximal SAR values were below 0.1 W kg(-1), far lower than the level at which thermal effects may occur, the adjusted odds ratios (ORs) for regular mobile phone users being 1.22 (95% confidence interval (CI): 0.63-2.37) for glioma and 0.70 (0.42-1.16) for meningioma. When the maximal SAR value inside the tumour tissue was accounted for in the exposure indices, the overall OR was again not increased and there was no significant trend towards an increasing OR in relation to SAR-derived exposure indices. A non-significant increase in OR among glioma patients in the heavily exposed group may reflect recall bias.     

Association of meningioma with reproductive factors

Meningiomas occur more commonly in females. The coincidence between meningioma and breast cancer and case reports of tumor growth during pregnancy support a hormonal hypothesis. A case control study was conducted to investigate this. Female subjects treated between 1987 and 1992 were identified from 3 hospitals in the Chicago area. Female spouses of male back pain patients were recruited as controls. A self-administered mail questionnaire focused on exogenous, endogenous and other hormonal factors, personal and family medical history as well as radiation exposures. Odds ratios and 95% confidence intervals were estimated using crude, stratified and multivariable logistic models including 219 cases and 260 controls. Participation rates were 86% among cases and 75% among controls. An increased odds ratio (OR) was observed comparing African Americans to Caucasians [OR = 2.4, 95% confidence interval (CI) = 1.0-6.1]. A protective effect was observed for pregnancy, which increased with number and age at first pregnancy. The odds ratio for 3 or more pregnancies compared to none was 0.3 (95% CI = 0.2-0.6). Age at menarche or total period of hormonal activity was not protective. Ever smokers showed a decreased odds ratio for meningioma (OR = 0.6, 95% CI = 0.4-0.9). The increased odds ratios with African Americans was retained in post-menopausal women, while the protective odds ratios for pregnancy, smoking and oral contraceptives (OCs) became stronger in pre-menopausal women. The pattern by duration and timing of use does not suggest an etiologic role for OCs or hormone replacement therapy. These data add to the evidence that factors known to influence endogenous hormones (pregnancy and indirectly smoking) may have protective effects for meningiomas primarily in premenopausal women.     

Risk of non-Hodgkin lymphoma and use of non-steroidal anti-inflammatory drugs

BACKGROUND: Risk factors for non-Hodgkin lymphoma (NHL) are largely unknown. Several studies have examined the relation of non-steroidal anti-inflammatory drug (NSAID) use to the risk of NHL, with inconsistent results. METHODS: We examined NSAID use among 529 newly diagnosed NHL cases and 2013 controls interviewed from 1977 to 2002 in our Case-Control Surveillance Study. RESULTS: The odds ratio for NHL among subjects whose regular NSAID use began at least one year prior to hospital admission compared to never users was 0.9 (95% confidence interval (CI): 0.6-1.3). Odds ratios for less than five years, five to less than 10 years, and 10 or more years of regular use were 1.2 (95% CI: 0.8-1.9), 1.0 (95% CI: 0.5-2.1), and 0.4 (95% CI: 0.1-1.0), respectively. The results were similar for regular aspirin use. CONCLUSION: Our results add to the body of data suggesting that NSAIDs do not increase the risk of NHL and even suggest the possibility of protection by long-term use.     

Cancer incidence in families with multiple glioma patients

Twenty-four Finnish families with 2 or more glioma patients were identified through questionnaires sent to 369 consecutive glioma patients receiving surgery at Tampere University Hospital during 1983-94. To explore whether unusual cancer susceptibility is involved, the cancer risk of 2,664 family members was estimated using population-based data from the Finnish Cancer Registry. Among the total cohort of relatives, 88 cancers were observed during 1953-97. The overall cancer risk among 12 families with juvenile onset gliomas was significantly decreased (standardized incidence ratio [SIR] 0.6, 95% confidence interval [CI]: 0.4-0.9). Among 12 families with adult onset gliomas, the overall cancer risk was equal to that of the reference population (SIR 1.1, 95% CI: 0.8-1.4) whereas the risk of skin melanoma (SIR 4.0, 95% CI: 1.5-8.8) and meningioma (SIR 5.5, 95% CI: 1.1-16) were significantly increased. Several other tumors, including those associated with neurofibromatosis 1 and 2, tuberous sclerosis and Li-Fraumeni and Turcot syndromes were surveyed, but no elevated risks were observed. In conclusion, the presence of meningiomas and skin melanomas in glioma families may indicate a novel association as a cancer susceptibility trait.     

Association between vestibular schwannomas and mobile phone use

Vestibular schwannomas (VSs) grow in the region where the energy from mobile phone use is absorbed. We examined the associations of VSs with mobile phone use. This study included 119 patients who had undergone surgical tumor removal. We used two approaches in this investigation. First, a case–control study for the association of mobile phone use and incidence of VSs was conducted. Both cases and controls were investigated with questions based on INTERPHONE guidelines. Amount of mobile phone use according to duration, daily amount, and cumulative hours were compared between two groups. We also conducted a case–case study. The location and volume of the tumors were investigated by MRI. Associations between the estimated amount of mobile phone use and tumor volume and between the laterality of phone use and tumor location were analyzed. In a case–control study, the odds ratio (OR) of tumor incidence according to mobile phone use was 0.956. In the case–case study, tumor volume and estimated cumulative hours showed a strong correlation (r ²?=?0.144, p?=?0.002), and regular mobile phone users showed tumors of a markedly larger volume than those of non-regular users (p?<?0.001). When the analysis was limited to regular users who had serviceable hearing, laterality showed a strong correlation with tumor side (OR?=?4.5). We found that tumors may coincide with the more frequently used ear of mobile phones and tumor volume that showed strong correlation with amount of mobile phone use, thus there is a possibility that mobile phone use may affect tumor growth.