PURPOSE: Case-control studies have reported inconsistent findings regarding the association between mobile phone use and tumor risk. We investigated these associations using a meta-analysis. METHODS: We searched MEDLINE (PubMed), EMBASE, and the Cochrane Library in August 2008. Two evaluators independently reviewed and selected articles based on predetermined selection criteria. RESULTS: Of 465 articles meeting our initial criteria, 23 case-control studies, which involved 37,916 participants (12,344 patient cases and 25,572 controls), were included in the final analyses. Compared with never or rarely having used a mobile phone, the odds ratio for overall use was 0.98 for malignant and benign tumors (95% CI, 0.89 to 1.07) in a random-effects meta-analysis of all 23 studies. However, a significant positive association (harmful effect) was observed in a random-effects meta-analysis of eight studies using blinding, whereas a significant negative association (protective effect) was observed in a fixed-effects meta-analysis of 15 studies not using blinding. Mobile phone use of 10 years or longer was associated with a risk of tumors in 13 studies reporting this association (odds ratio = 1.18; 95% CI, 1.04 to 1.34). Further, these findings were also observed in the subgroup analyses by methodologic quality of study. Blinding and methodologic quality of study were strongly associated with the research group. CONCLUSION: The current study found that there is possible evidence linking mobile phone use to an increased risk of tumors from a meta-analysis of low-biased case-control studies. Prospective cohort studies providing a higher level of evidence are needed.

Oral Diseases (2009) DOI: 10.1111/j.1601-0825.2009.01620.xBackground: Handheld mobile phones (MPHs) have become a 'cultural' accessory device, no less so than a wrist watch. Nevertheless, the use of MPHs has given rise to great concern because of possible adverse health effects from exposure to the radiofrequency radiation (RFR) emitted by the device. Previous studies suggested correlation between MPH and salivary gland tumors. Objective: To evaluate whether MPH induces physiologic changes in the adjacent parotid gland, located on the dominant side, in terms of secretion rates and protein levels in the secreted saliva. Materials and method: Stimulated parotid saliva was collected simultaneously from both glands in 50 healthy volunteers whose MPH use was on a dominant side of the head. Results: A significantly higher saliva secretion rate was noticed in the dominant MPH side compared with that in the non-dominant side. Lower total protein concentration was obtained in the dominant compared with the non-dominant MPH side among the right dominant MPH users. Conclusions: Parotid glands adjacent to handheld MPH in use respond by elevated salivary rates and decreased protein secretion reflecting the continuous insult to the glands. This phenomenon should be revealed to the worldwide population and further exploration by means of large-scale longitudinal studies is warranted.

This review summarizes and interprets epidemiologic evidence bearing on a possible causal relation between radiofrequency field exposure from mobile phone use and tumor risk. In the last few years, epidemiologic evidence on mobile phone use and the risk of brain and other tumors of the head in adults has grown in volume, geographic diversity of study settings, and the amount of data on longer-term users. However, some key methodologic problems remain, particularly with regard to selective nonresponse and inaccuracy and bias in recall of phone use. Most studies of glioma show small increased or decreased risks among users, although a subset of studies show appreciably elevated risks. We considered methodologic features that might explain the deviant results, but found no clear explanation. Overall the studies published to date do not demonstrate an increased risk within approximately 10 years of use for any tumor of the brain or any other head tumor. Despite the methodologic shortcomings and the limited data on long latency and long-term use, the available data do not suggest a causal association between mobile phone use and fast-growing tumors such as malignant glioma in adults (at least for tumors with short induction periods). For slow-growing tumors such as meningioma and acoustic neuroma, as well as for glioma among long-term users, the absence of association reported thus far is less conclusive because the observation period has been too short.

The fourth course at the International School of Bioelectromagnetics addressed various aspects of the epidemiology of exposure to electromagnetic fields (EMF). In this overview, inspired by the lectures and the discussions among participants, we summarize current knowledge on exposure to EMF and disease risk, with emphasis on studies of use of mobile phones and brain tumours and exposure to power lines and childhood leukaemia. Sources of bias and error hamper straightforward conclusions in some areas and, in order to move forward, improvements in study design and exposure assessment are necessary. The scientific evidence available to date on possible long-term effects from exposure to ELF and RF fields is not strong enough to revise current protection limits based on the known acute effects of such exposures. Precautionary measures may be considered to reduce ELF exposure of children or exposure to RF during mobile phone use, keeping in mind that it is unclear whether they involve any preventive benefit. Possible health effects from mobile phone use in adults and in children should be investigated further by prospective epidemiological studies with improved exposure assessment and brain tumour incidence rates should be monitored. Further studies on the relation between childhood leukaemia and ELF magnetic fields would be worthwhile if they focus on heavily exposed groups and attempt to minimize possible selection bias. In conclusion, epidemiological studies conducted with appropriate diligence can play a key role in finding the answers. Bioelectromagnetics, 2009.(c) 2009 Wiley-Liss, Inc.

OBJECTIVE: During the last decade, mobile phone use increased to almost 100% prevalence in many countries of the world. Evidence for potential health hazards accumulated in parallel by epidemiologic investigations has raised controversies about the appropriate interpretation and the degree of bias and confounding responsible for reduced or increased risk estimates. DATA SOURCES: Overall, I identified 33 epidemiologic studies in the peer-reviewed literature, most of which (25) were about brain tumors. Two groups have collected data for >/= 10 years of mobile phone use: Hardell and colleagues from Sweden and the Interphone group, an international consortium from 13 countries coordinated by the International Agency for Research on Cancer. DATA SYNTHESIS: Combined odds ratios (95% confidence intervals) from these studies for glioma, acoustic neuroma, and meningioma were 1.5 (1.2-1.8); 1.3 (0.95-1.9); and 1.1 (0.8-1.4), respectively. CONCLUSIONS: METHODOLOGIC CONSIDERATIONS REVEALED THAT THREE IMPORTANT CONDITIONS FOR EPIDEMIOLOGIC STUDIES TO DETECT AN INCREASED RISK ARE NOT MET: a ) no evidence-based exposure metric is available; b) the observed duration of mobile phone use is generally still too low; c) no evidence-based selection of end points among the grossly different types of neoplasias is possible because of lack of etiologic hypotheses. Concerning risk estimates, selection bias, misclassification bias, and effects of the disease on mobile phone use could have reduced estimates, and recall bias may have led to spuriously increased risks. The overall evidence speaks in favor of an increased risk, but its magnitude cannot be assessed at present because of insufficient information on long-term use.

BACKGROUND: The debate regarding the health effects of low-intensity electromagnetic radiation from sources such as power lines, base stations, and cell phones has recently been reignited. In the present review, the authors attempt to address the following question: is there epidemiologic evidence for an association between long-term cell phone usage and the risk of developing a brain tumor? Included with this meta-analysis of the long-term epidemiologic data are a brief overview of cell phone technology and discussion of laboratory data, biological mechanisms, and brain tumor incidence. METHODS: In order to be included in the present meta-analysis, studies were required to have met all of the following criteria:(i) publication in a peer-reviewed journal;(ii) inclusion of participants using cell phones for >/=10 years (ie, minimum 10-year "latency"); and (iii) incorporation of a "laterality" analysis of long-term users (ie, analysis of the side of the brain tumor relative to the side of the head preferred for cell phone usage). This is a meta-analysis incorporating all 11 long-term epidemiologic studies in this field. RESULTS: The results indicate that using a cell phone for >/=10 years approximately doubles the risk of being diagnosed with a brain tumor on the same ("ipsilateral") side of the head as that preferred for cell phone use. The data achieve statistical significance for glioma and acoustic neuroma but not for meningioma. CONCLUSION: The authors conclude that there is adequate epidemiologic evidence to suggest a link between prolonged cell phone usage and the development of an ipsilateral brain tumor.

Mobile telecommunication technology became commercially available about 20-25 years ago in different countries around the world. The industry has grown exponentially over the years and, currently, the number of mobile phone users is estimated to be over 3.8 billion, more than half the world's population. Thus, because of such a large population-at-risk, any health hazard from these devices promises to have a large epidemiological impact. Intense speculation and investigation into the relationship between mobile phone usage and cancer has led to the publication of numerous, often contradictory, reports on this subject. This review aims to provide a large body of reported evidence to help medical professionals disseminate evidence-based information to their patients.

The aim of this study was to explore the prevalence, nature and determinants of concerns about mobile phone radiation. We used data from a 2006 telephone survey of 1004 people aged 15+ years in Denmark. Twenty-eight percent of the respondents were concerned about exposure to mobile phone radiation; radiation from masts was of concern to about 15%. In contrast, 82% were concerned about pollution. Nearly half of the respondents considered the mortality risk of 3G phones and masts to be of the same order of magnitude as being struck by lightning (0.1 fatalities per million people per year) while 7% thought it was equivalent to tobacco-induced lung cancer ( approximately 500 fatalities per million per year). Among women, concerns about mobile phone radiation were positively associated with educational attainment, perceived mobile phone mortality risk and concerns about unknown consequences of new technologies. More than two thirds of the respondents felt that they had received inadequate public information about the 3G system. The results of the study indicate that the majority of the population has little concern about mobile phone radiation while a small minority is very concerned. Bioelectromagnetics, 2009 (c) 2009 Wiley-Liss, Inc.

Global exposures to emerging wireless technologies from applications including mobile phones, cordless phones, DECT phones, WI-FI, WLAN, WiMAX, wireless internet, baby monitors, and others may present serious public health consequences. Evidence supporting a public health risk is documented in the BioInitiative Report. New, biologically based public exposure standards for chronic exposure to low-intensity exposures are warranted. Existing safety standards are obsolete because they are based solely on thermal effects from acute exposures. The rapidly expanding development of new wireless technologies and the long latency for the development of such serious diseases as brain cancers means that failure to take immediate action to reduce risks may result in an epidemic of potentially fatal diseases in the future. Regardless of whether or not the associations are causal, the strengths of the associations are sufficiently strong that in the opinion of the authors, taking action to reduce exposures is imperative, especially for the fetus and children. Such action is fully compatible with the precautionary principle, as enunciated by the Rio Declaration, the European Constitution Principle on Health (Section 3.1) and the European Union Treaties Article 174.

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.

BACKGROUND: Because existing data regarding the relation between smoking and salivary gland tumors are sparse, tobacco is currently not classified as a salivary gland carcinogen. The objective of the current study was to assess the association between smoking and benign and malignant parotid gland tumors (PGTs) in a nationwide study. METHODS: The sample included 459 patients with incident PGT, aged >/=18 years, who were diagnosed between 2001 and 2003 and a group of 1265 individually matched, population-based controls. Analyses of the risk of PGT associated with various smoking variables were performed by using conditional logistic regression. Data also were stratified by histologic type; statistical significance tests were 2-sided. RESULTS: Ever smoking cigarettes was associated with an odds ratio (OR) of 1.66 (95% confidence interval [95% CI], 1.31-2.11) for developing a PGT. The risk was strongest for early ages at smoking initiation, and trends of increasing risk were observed with increasing smoking intensity, pack-years, latent period, and smoking duration (P for trend <.001 for each). Analysis by histologic type indicated remarkably high risks for Warthin tumor (OR for ever cigarette smokers: 15.3; 95% CI, 6.1-38.5). For pleomorphic adenomas and malignant tumors, the risks associated with ever smoking were 1.01 (95% CI, 0.75-1.37) and 1.69 (95% CI, 0.81-3.51), respectively. CONCLUSIONS: Smoking plays an important role in the development of Warthin tumor. Although no association was observed for pleomorphic adenoma, the possible indication of increased risk of malignant tumors requires further investigation in larger studies. Cancer 2008.(c) 2008 American Cancer Society.

The very rapid worldwide increase in mobile phone use in the last decade has generated considerable interest in the possible health effects of exposure to radio frequency (RF) fields. A multinational case-control study, INTERPHONE, was set-up to investigate whether mobile phone use increases the risk of cancer and, more specifically, whether the RF fields emitted by mobile phones are carcinogenic. The study focused on tumours arising in the tissues most exposed to RF fields from mobile phones: glioma, meningioma, acoustic neurinoma and parotid gland tumours. In addition to a detailed history of mobile phone use, information was collected on a number of known and potential risk factors for these tumours. The study was conducted in 13 countries. Australia, Canada, Denmark, Finland, France, Germany, Israel, Italy, Japan, New Zealand, Norway, Sweden, and the UK using a common core protocol. This paper describes the study design and methods and the main characteristics of the study population. INTERPHONE is the largest case-control study to date investigating risks related to mobile phone use and to other potential risk factors for the tumours of interest and includes 2,765 glioma, 2,425 meningioma, 1,121 acoustic neurinoma, 109 malignant parotid gland tumour cases and 7,658 controls. Particular attention was paid to estimating the amount and direction of potential recall and participation biases and their impact on the study results.

Ionizing radiation is an established risk factor for brain tumors, yet quantitative information on the long-term risk of different types of brain tumors is sparse. Our aims were to assess the risk of radiation-induced malignant brain tumors and benign meningiomas after childhood exposure and to investigate the role of potential modifiers of that risk. The study population included 10,834 individuals who were treated for tinea capitis with X rays in the 1950s and two matched nonirradiated groups, comprising population and sibling comparison groups. The mean estimated radiation dose to the brain was 1.5 Gy. Survival analysis using Poisson regression was performed to estimate the excess relative and absolute risks (ERR, EAR) for brain tumors. After a median follow-up of 40 years, an ERR/Gy of 4.63 and 1.98 (95% CI = 2.43-9.12 and 0.73-4.69) and an EAR/Gy per 10(4) PY of 0.48 and 0.31 (95% CI = 0.28-0.73 and 0.12-0.53) were observed for benign meningiomas and malignant brain tumors, respectively. The risk of both types of tumors was positively associated with dose. The estimated ERR/Gy for malignant brain tumors decreased with increasing age at irradiation from 3.56 to 0.47 (P = 0.037), while no trend with age was seen for benign meningiomas. The ERR for both types of tumor remains elevated at 30-plus years after exposure.

PURPOSE: To quantitatively assess the impact of selection bias caused by nonparticipation in a multinational case-control study of mobile phone use and brain tumor. METHODS: Non-response questionnaires (NRQ) were completed by a sub-set of nonparticipants. Selection bias factors were calculated based on the prevalence of mobile phone use reported by nonparticipants with NRQ data, and on scenarios of hypothetical exposure prevalence for other nonparticipants. RESULTS: Regular mobile phone use was reported less frequently by controls and cases who completed the NRQ (controls, 56%; cases, 50%) than by those who completed the full interview (controls, 69%; cases, 66%). This relationship was consistent across study centers, sex, and age groups. Lower education and more recent start of mobile phone use were associated with refusal to participate. Bias factors varied between 0.87 and 0.92 in the most plausible scenarios. CONCLUSIONS: Refusal to participate in brain tumor case-control studies seems to be related to less prevalent use of mobile phones, and this could result in a downward bias of around 10% in odds ratios for regular mobile phone use. The use of simple selection bias estimation methods in case-control studies can give important insights into the extent of any bias, even when nonparticipant information is incomplete.

Background: The thyroid gland is known to be sensitive to the carcinogenic effect of ionizing radiation, especially in children. The role of potential modifiers of the risk, and latency period effects, need further investigation. We examined the effect of low doses of ionizing radiation (4.5-49.5cGy) on the risk of developing thyroid cancer after long latent periods of up to 54 yr following childhood exposure. Methods: The study population included 10,834 individuals irradiated against Tinea Capitis in the 1950s, and two matched non-irradiated groups (general population and siblings) for comparison. Cancer statistics and vital status data were obtained from national registries, updated to December 2002. Excess relative and absolute risks (ERR, EAR) were estimated using Poisson regression for survival analysis. Results: Within the study period 159 cases of thyroid cancer were diagnosed. Total ERR/Gy and EAR/Gy/10(4) PY for developing thyroid cancer reached 20.2 (95% CI = 11.8-32.3) and 9.9 (95% CI=5.7-14.7) respectively. The risk was positively associated with dose, and negatively associated with age at exposure. ERR/Gy was significantly elevated 10-19 yr following exposure, peaking at 20-30 yr, and decreasing dramatically (although still significantly elevated) 40 yr after exposure. Conclusions: Our findings agree with patterns of risk modification seen in most studies of radiation-induced thyroid cancer, although risk per unit dose seems higher. Our data show that 40 yr after irradiation ERR decreases dramatically, though remaining significantly elevated. The hypothesis of different genetic susceptibility of the Jewish population deserves further exploration.

BACKGROUND: Skeletal nasal changes in elderly people have been extensively investigated, but data on variation of the endonasal architecture with age do not exist. We evaluated endonasal parameters in an elderly population as compared with those in a young group. METHODS: Acoustic rhinometry measurements were performed on 165 participants in the age range of 20-93 years. The rhinograms provided the endonasal volume from the nostril entrance to a 7.0 cm cephalic point (V0-7) and the minimal cross-sectional areas (MCA1 and MCA2). Statistical analysis was performed by Pearson correlation and one-way analysis of variance, using age as a continuous or categorical variable. RESULTS: There was no statistical difference in gender distribution within each age group. The results obtained for the left and right nostrils were similar. Endonasal volume V0-7 and the narrowing areas MCA1 and MCA2 significantly increase with age, except for men over 80 years in which a relative decrease was observed. CONCLUSION: Acoustic rhinometry examination of the endonasal architecture in a healthy young and elderly population demonstrated a gradual increase of endonasal volumes and minimal cross-sectional areas with age.

OBJECTIVES:: To evaluate the incidence rates of cervical cancer by ethnic origins and compare these rates between first- and second-generation women of North African origin. METHODS:: Data of all cervical carcinoma of Jewish women during 2000 to 2005 were obtained from the National Cancer Registry. Standardized incidence ratios for each ethnic origin category were calculated and compared using Poisson regression. RESULTS:: During the study period, 938 patients were examined. The standardized incidence ratios of North African-born women and of Israeli-born women of North African descent were significantly higher compared with those of women of other origins. CONCLUSIONS:: The persistence of a higher risk of cervical cancer in Israeli Jewish women of North African descent compared with those of other origins may suggest that genetic factors are involved in the etiology of this neoplasm.

OBJECTIVE: Although causal relationships between smoking and cancer risk have been established for many sites, most studies of brain cancer have not supported an association. However, two recent cohort studies showed increased risks of glioma among smokers. We quantified the association between smoking and glioma through a meta-analysis of the literature. METHODS: Of 20 eligible studies, 17 (6 cohort and 11 case-control) were included in an analysis of ever versus never smoking. Multivariate-adjusted risk estimates in the papers were pooled to calculate cumulative risk. RESULTS: The cumulative estimated risk associated with ever smoking was 1.06 (95% CI: 0.97-1.15), for all, 1.10 (95% CI: 1.01-1.20) for cohort, and 1.00 (95% CI: 0.88-1.15) for case-control studies. A significantly increased risk associated with past smoking was noted for cohort studies, OR = 1.16 (p = 0.007), while an increased risk of borderline significance was seen for all studies, OR = 1.10 (p = 0.08). In general, dose-response analysis did not support an association and was limited because very few studies included these variables and could be pooled. CONCLUSION: Overall, results of pooling of all studies suggested that smoking is not associated with risk of glioma. However, the small but significant increased risk seen for cohort studies remains to be clarified.

PURPOSE: To assess the association between duration of symptoms and main prognostic factors of invasive epithelial ovarian cancer (EOC). METHODS: The data of all histologically confirmed EOC patients diagnosed in Israel during the period 1994-1999 (n = 1,005) were retrieved from discharge summaries and admission records. Of the 371 (36.9%) patients with known presenting symptoms, the durations of 187 (50.4%) were recorded. RESULTS: The most common presenting symptoms were abdominal pain (65.2%). The percentage of patients with three or more symptoms increased significantly with stage (P = 0.001). No statistically significant association between duration of symptoms and prognostic factors was found. CONCLUSION: Our findings did not show an association between duration of symptoms and prognostic factors in EOC patients and may indicate that prognosis is not a function of delay in diagnosis.

Background: Glial brain tumors span a wide range of neoplasms with distinct clinical and histopathological features. This report presents the descriptive epidemiology of glial tumors by histological subtype and tumor behavior. Methods: The study population included all incident cases of glial tumors diagnosed in Israel during March 2001 to July 2003. Age-standardized incidence rates (ASR) were calculated using the world population as a standard. Results: A total of 548 tumors were diagnosed, of which 520 had histological confirmation. The ASR of all adult (>20 years) glial tumors was 5.82/100,000 (7.11 for males; 4.75 for females, p < 0.001). The majority of tumors (78%) were classified as high grade; astrocytic tumors were the most frequent (85%), with glioblastoma multiforme accounting for 70% of them. A significant positive association was shown between age at diagnosis and grade. The highest ASR was seen for Europe- and-American-born, followed by Israeli, Asian and African-born individuals (6.78, 5.86, 4.94 and 3.84/100,000, respectively). Conclusions: In general, these results describing data of incident cases of pathologically validated glial tumors are consistent with previous reports. To enhance our understanding of these diseases, epidemiological studies should rely on well-defined histological tumor types, incorporating comprehensive information which will allow comparability between different groups of patients.

In a large nationwide cohort study including 420,095 persons whose first mobile phone subscription was between 1982 and 1995, who were followed through 2003 for hospital contacts for a diagnosis of a central nervous system disease, we observed 10-20% more hospital contacts than expected for migraine and vertigo and 30-40% less hospital contacts than expected for dementia (Alzheimer's disease, vascular and other dementia), Parkinson's disease and epilepsy among men. No associations were seen for amyotrophic lateral sclerosis, multiple sclerosis or epilepsy in women.

This paper reviews the results of early cellphone studies, where exposure duration was too short to expect tumorigenesis, as well as two sets of more recent studies with longer exposure duration: the Interphone studies and the Swedish studies led by Dr. Lennart Hardell. The recent studies reach very different conclusions. With four exceptions the industry-funded Interphone studies found no increased risk of brain tumors from cellphone use, while the Swedish studies, independent of industry funding, reported numerous findings of significant increased brain tumor risk from cellphone and cordless phone use. An analysis of the data from the Interphone studies suggests that either the use of a cellphone protects the user from a brain tumor, or the studies had serious design flaws. Eleven flaws are identified:(1) selection bias,(2) insufficient latency time,(3) definition of 'regular' cellphone user,(4) exclusion of young adults and children,(5) brain tumor risk from cellphones radiating higher power levels in rural areas were not investigated,(6) exposure to other transmitting sources are excluded,(7) exclusion of brain tumor types,(8) tumors outside the cellphone radiation plume are treated as exposed,(9) exclusion of brain tumor cases because of death or illness,(10) recall accuracy of cellphone use, and (11) funding bias. The Interphone studies have all 11 flaws, and the Swedish studies have 3 flaws (8, 9 and 10). The data from the Swedish studies are consistent with what would be expected if cellphone use were a risk for brain tumors, while the Interphone studies data are incredulous. If a risk does exist, the public health cost will be large. These are the circumstances where application of the Precautionary Principle is indicated, especially if low-cost options could reduce the absorbed cellphone radiation by several orders of magnitude.

OBJECTIVE: During the last decade, mobile phone use increased to almost 100% prevalence in many countries of the world. Evidence for potential health hazards accumulated in parallel by epidemiologic investigations has raised controversies about the appropriate interpretation and the degree of bias and confounding responsible for reduced or increased risk estimates. DATA SOURCES: Overall, I identified 33 epidemiologic studies in the peer-reviewed literature, most of which (25) were about brain tumors. Two groups have collected data for >/= 10 years of mobile phone use: Hardell and colleagues from Sweden and the Interphone group, an international consortium from 13 countries coordinated by the International Agency for Research on Cancer. DATA SYNTHESIS: Combined odds ratios (95% confidence intervals) from these studies for glioma, acoustic neuroma, and meningioma were 1.5 (1.2-1.8); 1.3 (0.95-1.9); and 1.1 (0.8-1.4), respectively. CONCLUSIONS: METHODOLOGIC CONSIDERATIONS REVEALED THAT THREE IMPORTANT CONDITIONS FOR EPIDEMIOLOGIC STUDIES TO DETECT AN INCREASED RISK ARE NOT MET: a ) no evidence-based exposure metric is available; b) the observed duration of mobile phone use is generally still too low; c) no evidence-based selection of end points among the grossly different types of neoplasias is possible because of lack of etiologic hypotheses. Concerning risk estimates, selection bias, misclassification bias, and effects of the disease on mobile phone use could have reduced estimates, and recall bias may have led to spuriously increased risks. The overall evidence speaks in favor of an increased risk, but its magnitude cannot be assessed at present because of insufficient information on long-term use.

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.

BACKGROUND: Tinnitus is a frequent condition with high morbidity and impairment in quality of life. The pathophysiology is still incompletely understood. Electromagnetic fields are discussed to be involved in the multi-factorial pathogenesis of tinnitus, but data proofing this relationship are very limited. Potential health hazards of electromagnetic fields (EMF) have been under discussion for long. Especially, individuals claiming themselves to be electromagnetic hypersensitive suffer from a variety of unspecific symptoms, which they attribute to EMF-exposure. The aim of the study was to elucidate the relationship between EMF-exposure, electromagnetic hypersensitivity and tinnitus using a case-control design. METHODOLOGY: Tinnitus occurrence and tinnitus severity were assessed by questionnaires in 89 electromagnetic hypersensitive patients and 107 controls matched for age-, gender, living surroundings and workplace. Using a logistic regression approach, potential risk factors for the development of tinnitus were evaluated. FINDINGS: Tinnitus was significantly more frequent in the electromagnetic hypersensitive group (50.72% vs. 17.5%) whereas tinnitus duration and severity did not differ between groups. Electromagnetic hypersensitivity and tinnitus were independent risk factors for sleep disturbances. However, measures of individual EMF-exposure like e.g. cell phone use did not show any association with tinnitus. CONCLUSIONS: Our data indicate that tinnitus is associated with subjective electromagnetic hypersensitivity. An individual vulnerability probably due to an over activated cortical distress network seems to be responsible for, both, electromagnetic hypersensitivity and tinnitus. Hence, therapeutic efforts should focus on treatment strategies (e.g. cognitive behavioral therapy) aiming at normalizing this dysfunctional distress network.

BACKGROUND:: There is public concern and scientific interest regarding a potential effect of cellular phone use on the risk of developing intracranial tumors. Tumors of the pituitary gland have barely been investigated in this context, but are of interest because of their intracranial location. METHODS:: We conducted a population-based case-control study between 2001 and 2005 of the risk of developing pituitary tumors in relation to cellular phone use in Southeast England, with 291 cases and 630 controls. Detailed information on cellular phone use was collected by personal interview. RESULTS:: Tumor risk was not associated with cellular phone use overall (adjusted odds ratio = 0.9, 95% confidence interval = 0.7-1.3), and was not appreciably increased 10 or more years after first use (1.0; 0.5-1.9), or after 10 or more years of cumulative use (1.1; 0.5-2.4). Odds ratios were 1.2 (0.7-1.9) for users in the highest quartile of cumulative number of calls and 1.1 (0.7-1.7) in the highest quartile of hours of use. Separate analyses of analog and digital phone use showed no associations with tumor risk. CONCLUSIONS:: We found no evidence that the risk of developing pituitary tumors is associated with cellular phone use for the induction time periods and intensities of use observed.

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.

OBJECTIVE: To explore polarization of T lymphocyte and its relationship with apoptosis of marrow cells in patients with myelodysplastic syndromes (MDS). METHODS: Measurements of Th1, Th2, Tc1, Tc2 subsets in bone marrows from 34 patients with MDS and 13 normal controls were performed by flow cytometry. INF-gamma and TNF-alpha in marrow serum were determined by ELISA (Enzyme-linked immunosorbent assay). Apoptosis index of marrow cells was detected by TUNEL (TdT-mediated dUTP nick end labeling). Correlations between Th1, Th2, Tc1, Tc2 subsets and INF-gamma, TNF-alpha levels as well as apoptosis index were analyzed, and relationship between TNF-alpha, INF-gamma levels and apoptosis index was also investigated. RESULTS:(1) The percentage of Th1 cells [(10.1 +/- 1.6)%], Tc1 cells [(24.0 +/- 3.6)%] and Tc1/Tc2 ratio (50.0 +/- 11.1) was significantly increased in patients with MDS than in normal controls [(4.0 +/- 0.5)%,(5.8 +/- 0.6)% and 13.4 +/- 2.7, respectively]. Levels of INF-gamma [(58.6 +/- 21.7) microg/L] and TNF-alpha [(15.7 +/- 3.8) microg/L] in marrow serum of MDS patients was markedly elevated compared to normal controls [0 and (0.3 +/- 0.2) microg/L, respectively]. An increased apoptosis index of nucleated cells was observed in MDS patients [(7.8 +/- 1.5)%] as compared to controls [(2.1 +/- 0.3)%, P < 0.05]. The Th1 cell percentage showed a positive correlation with the levels of INF-gamma and TNF-alpha (r = 0.38, P < 0.05 and r = 0.39, P < 0.05, respectively), and with apoptotic index of nucleated marrow cells in MDS patients (r = 0.33, P < 0.05). Furthermore, a positive correlation was observed between INF-gamma, TNF-alpha levels and apoptotic index of marrow cells (r = 0.74, P < 0.01 and r = 0.73, P < 0.01, respectively).(2) Th1, Tc1 cells and Tc1/Tc2 ratio in MDS-RCMD patients was markedly elevated (P < 0.01) but did not in RCMD-RS, RAEB-1 and RAEB-2 patients as compared to normal controls.(3) An elevation in the percentages of Th1, Tcl and Tc1/ Tc2 ratio was detected in patients with IPSS lower-risk but did not in higher-risk group as compared to controls.(4) Increased Th1 and Tc1 percentages and Th1/Th2 and Tc1/Tc2 ratios were observed in RCMD patients with normal karyotype, but did not in those with abnormal karyotype. Conclusions Th1/Th2 and Tc1/Tc2 in bone marrow of MDS patients were unbalanced, polarizing to type I reaction especially in patients with RCMD subtype, IPSS lower-risk and normal karyotype. The increased Th1 cells in bone marrow may account for the increased apoptosis of nucleated marrow cells in MDS, through proapoptotic cytokines such as INF-gamma and TNF-alpha.

The objective of this nationwide study was to assess the association between cellular phone use and development of parotid gland tumors (PGTs). The methods were based on the international INTERPHONE study that aimed to evaluate possible adverse effects of cellular phone use. The study included 402 benign and 58 malignant incident cases of PGTs diagnosed in Israel at age 18 years or more, in 2001-2003, and 1,266 population individually matched controls. For the entire group, no increased risk of PGTs was observed for ever having been a regular cellular phone user (odds ratio = 0.87; p = 0.3) or for any other measure of exposure investigated. However, analysis restricted to regular users or to conditions that may yield higher levels of exposure (e.g., heavy use in rural areas) showed consistently elevated risks. For ipsilateral use, the odds ratios in the highest category of cumulative number of calls and call time without use of hands-free devices were 1.58 (95% confidence interval: 1.11, 2.24) and 1.49 (95% confidence interval: 1.05, 2.13), respectively. The risk for contralateral use was not significantly different from 1. A positive dose-response trend was found for these measurements. Based on the largest number of benign PGT patients reported to date, our results suggest an association between cellular phone use and PGTs.