ICES Database ElectroMagnetic Field Literature Search Engine |
 |
| |
| Home |
| View EMF Studies (Static,ELF) 0-300 Hz |
| View EMF Studies (Intermediate) 300 Hz-300 KHz |
| View EMF Studies (RF/mmW/THz) 300 kHz-300 GHz |
| Advanced Search |
| Citation List (Author Search) |
(Database last updated on Mar 27, 2024)
| ID Number | 229 | |
| Study Type | Epidemiology | |
| Model | 450, 900, 1800 MHz (NMT, GSM) mobile and cordless phone use and correlation with brain, salivary gland, acoustic neuroma, testicular, and lymphatic cancers plus RF exposure measurements. | |
| Details | Two large case control studies and numerous subsequent analyses were performed to evaluate correlations between brain tumors (identified from cancer registries of the Regional Oncology Center in Sockholm and Uppsala-Orebro regions ) and mobile phone use. In an initial report of 209 cases + 425 controls with brain tumors (recorded January 1997 to June 2000), the authors reported no significant increase in tumor incidence (either malignant or benign) with either analogue or digital cellular telephone exposure [GSM+NMT] OR=0.98; 95%CI 0.69-1.41), [GSM only] OR=0.96; [NMT only] OR=0.93). The authors did report an association between NMT (but not GSM) exposure and ipsilateral tumors using a multivariate analysis (OR=2.45). In subsequent papers, an expanded analysis was performed that included 1617 additional brain tumor cases and employed different statistical methods. In these studies, a significant association was reported for NMT use and benign acoustic neuromas (OR 4.4, 95% CI=2.1-9.2), but not with malignant tumors, and no associations were found between benign or malignant tumors and GSM use. These initial studies also reported an association between NMT use and total brain tumors (OR 1.3, 95% CI 1.04-1.6), although this was mainly due to the influence of the elevated benign tumors (analyzed separately there was no association between NMT use and malignant tumors alone). With further evaluation, ipsilateral brain tumors were found associated with NMT use (OR 1.7, 95% CI 1.2-2.3) as well as with GSM (OR 1.3, 95% CI 1.02-1.8) use. In subsequent papers with more re-analysis, ipsilateral astrocytomas (malignant tumors) were now found correlated with NMT use (OR=1.8, 95% CI 1.1-3.2), as well as with GSM use (OR=1.8, 95% CI=1.1-2.8), and cordless phone use (OR=1.8, 95% CI=1.1-2.9). Ipsilateral tumors located specifically in the temporal area of the brain were correlated even stronger with NMT use (OR=2.3, 95% CI=1.2-4.1). Mobile phone use on the opposite (contralateral) side of the brain was not associated with increased risk for any type of brain tumor. The authors also reported a shorter ipsilateral tumor induction period with exposure than for contralateral tumors, and hypothesized a tumor promoting effect of mobile phones. In another study (Neuroepidemiology, 2003, 22: 124-129), the same study group was further analyzed and the authors reported an association between analogue mobile phone use and vestibular schwannoma (OR 3.45, 95% CI 1.77-6.76). The vestibular schwannoma findings were suggested to correlate with reports by Oftedal et al and Sandstrom et al of increased complaints of tinnitus (a precondition of vestibular schwannoma) with mobile phone use in Norway, and a subsequent report by the authors described 3 additional cases of mobile phone users complaining of tinnitus that "contacted" them. A subsequent report (Occupational Environmental Medicine (2004) 61(8):675-9) using the same protocol and cancer registry reported no association between mobile or cordless phone use and salivary gland tumors, although the scarcity of this tumor type (only 0.2 percent tumors reported to the Swedish cancer registry in 2001) made statistical evaluation difficult. Another subsequent study (Occup Environ Med (2005) 62:390-394) looked at the same cases used above for correlations between brain tumors and urban (n=984 cases, 1035 controls) vs. rural (n=445 cases, n=435 controls) mobile phone use. The authors report a general correlation between total risk for all (malignant + benign) brain tumors and NMT analogue mobile phone use in urban (OR = 1.5; 95% CI 0.9 - 2.6) and rural (OR = 1.9; 95% CI 0.9 - 3.9) areas. For ipsilateral brain tumors (same side as mobile phone use) with a > 1 year latency, there was a slightly stronger correlation with analogue mobile phone use in urban areas (OR=1.7; 95% CI 1.1-2.5). A stronger correlation existed for ipsilateral brain tumors with a >5 year tumor latency and > 55 hours on the phone and rural residence (OR = 4.2; 95% CI 1.1-16). Associations between digital (GSM) phone and malignant brain tumors were higher for rural users than for urban users, especially when only ipsilateral tumors were considered (rural OR = 3.2; 95% CI 1.2 - 8.4 vs. urban OR = 0.9; 95% CI 0.6 - 1.4). When malignant brain tumors having >5 year tumor latency were considered, digital (GSM) mobile phone use in rural areas (OR=8.4; 95% CI 1.02-69) was more highly correlated than with urban use (OR = 1.4; 95% CI 0.8 - 2.6). The authors suggest that higher average transmit power of mobile phones in rural areas (presumably due to weaker receive signal from less dense base station sites and corresponding higher handset power) is responsible for increased correlations in rural areas. When 2000+ hrs of cumulative use was considered, OR = 5.9; 95% CI 2.5-14 for analog, OR = 3.7; 95% CI 1.7-7.7 for digital, and OR = 2.3; 95% CI 1.5-3.6 for cordless phone use. Additional reports (Neuroepidemiology 2005, 25:120-128) analyzed correlations between mobile and cordless phone use and various benign brain tumors (including 305 meningioma cases, 84 acoustic neuroma cases, 24 other benign tumor types, and 692 controls) in more detail. The authors report correlations between meningioma with a 10 year latency period and analogue mobile phone use (OR = 2.1; 95% CI = 1.1-4.3) as well as acoustic neuroma with analogue (OR = 4.2; 95% CI = 1.8-10) and digital (OR = 2.0; 95% CI = 1.05-3.8) mobile phone use. The risk between analogue mobile phone use and acoustic neuroma increased when a >15-year latency period was considered (OR = 8.4; 95% CI = 1.6-45) although this was based on low numbers. In a recent study (Environ Res 2005), the authors report additional data from malignant brain tumor cases (n = 317 + 692 controls) and report correlations with analogue mobile phone use (OR = 2.6; 95% CI 1.5 4.3, increasing to OR= 3.5; 95% CI 2.0 6.4 with a >10-year latency period) and digital mobile phone use (OR= 1.9; 95% CI = 1.3 2.7, increasing to OR = 3.6; 95% CI = 1.7 7.5 with a >10-year latency period). Correlations with cordless telephone use were also reported (OR = 2.1; 95% CI = 1.4 3.0, increasing to OR = 2.9; 95% CI = 1.6 5.2 with a >10-year latency period). The strongest correlation was with high grade astrocytoma. In a recent study reported in Int Arch Environ Health (2005) using the same questionnaire based exposure assessment and the same Swedish cancer registry population pool, the authors examine possible correlations with lymphoma (n = 910; 819 B-cell NHL, 53 T-cell NHL, 38 unspecified). They perform many different analyses and divide / stratify cases and controls by phone type, cancer sub-type, etc. They report no correlation between either NMT/analogue and GSM/digital mobile phone use and B-cell NHL, but a statistically significant correlation with T-cell NHL (OR = 2.47; 95% CI 1.09-5.60) based on 17 cases. They also report a correlation with cordless phone use for more than 10 years (OR = 3.15; 95% CI 1.05 - 9.48) based on 6 cases. Other correlations with stratified groups were also reported. In an earlier study (Epidemiology, 1999, 10:785-786) the authors reported angiosarcoma of the scalp associated with use of cordless telephones. An earlier report (Int. J. Oncol. 1998, 13:1299-1303 also reported possible associations between testicular cancer and amateur radio operators (OR 2.2; CI 0.7-6.6), work with radar equipment (OR 2.0; CI 0.3-14.2) and engineers in electronics and telecommunication industry (OR 2.3; CI 0.8-6.7), but this was based on very few exposed subjects. A review article was also reported by the authors (European J Cancer Prevention (2005) 14(3):285-288) describing their rationale and methods for combining different types of wireless phone (analog, cordless, GSM digital) to reflect an individual's RF exposure over time. A subsequent paper (Int J Oncol 2006) reported on the collective / pooled analysis from all of the tumor cases obtained between 1997 2003, which involved two separate case control studies with 1,254 cases / 2,162 controls and substantial analysis / reanalysis of the data. In this paper, the authors report correlations between acoustic neuroma and analogue mobile phone (OR = 2.9; 95% CI 2.0-4.3), GSM mobile phone (OR=1.5; 95% CI=1.1-2.1), and cordless telephone (OR=1.5, 95% CI=1.04-2.0) use. Analogue mobile phone use for >15 years gave the highest correlation (OR=3.8, 95% CI=1.4-10). The authors also report correlations between meningioma (a form of glioma) and analogue mobile phone (OR=1.3, 95% CI=0.99-1.7), GSM mobile phone (OR=1.1, 95% CI=0.9-1.3), and cordless telephone (OR=1.1, 95% CI=0.9-1.4) use. In particular, the authors identify that their reports on correlations between mobile phone exposure and iplilateral glial are supported by recent INTERPHONE reports, particularly the Hepworth et al 2006 paper. Three subsequent papers on meta-analysis of previously published studies (2 cohort + 16 case control) were performed (2007, 2008,, 2009) on 2946 brain tumors and the authors report the following: OR = 0.9; 95% CI 0.8-1.1 overall glioma, OR = 1.2; 95% CI 0.8-1.9 10+yr glioma, OR = 2.0; 95% CI 1.2-3.4 10+yr / ipsilateral glioma (4 studies total), OR = 0.9; 95% CI 0.7-1.1 overall acoustic neuroma, OR = 1.3; 95% CI 0.6-2.8 10+ yr acoustic neuroma, OR = 2.4; 95% CI 1.1-5.3 10+ yr / ipsilateral acoustic neuroma. In a set of earlier papers, the authors report no effects on testicular cancer with either mobile or cordless phone use. Although not yet published, the authors announced in a meeting organized by the Radiation Research Trust an increased correlation specifically between astrocytoma (OR = 1.4; 95% CI = 1.1-1.7) that increased with ipsilateral (OR = 2.0; 95% CI = 1.5-2.5), 10+ yr use (OR = 3.3; 95% CI = 2.0-5.4), and use prior to the age of 20 (OR = 5.2; 95% CI= 2.2-12.0). In a 2009 report, the authors evaluated 905 malignant brain tumor cases, 1254 benign brain tumor cases, and 2162 controls and reported OR = 1.4; 95% CI 1.1-1.7 for overall astrocytoma (grade I-IV), OR = 20; 95% CI 1.5-2.5 for ipsilateral astrocytoma (grade I-IV), and OR = 1.0; 95% CI 0.7-1.4 for contralateral astrocytoma (grade I-IV), OR = 2.7; 95% CI 1.8-3.9 for 10+yr astrocytoma, OR = 3.3; 95% CI 2.0-5.4 for ipsilateral astrocytoma, and OR = 2.8 (95% CI 1.5-5.1 contralateral astrocytoma. For cordless phones, OR = 1.4; 95% CI 1.1-1.8 for overall astrocytoma, OR = 1.8; 95% CI 1.4-2.4 for ipsilateral astrocytoma, and OR = 1.2 ; 95% CI 0.8-1.6 for contralateral astrocytoma, OR = 2.5 ; 95% CI 1.4-4.4 for 10+yr astrocytoma, OR = 5.0; 95% CI 2.3-11 for 10+yr ipsilateral astrocytoma, OR = 1.4; 95% CI 0.6-3.5 for 10+yr contralateral astrocytoma. ORs analyzed separately by age group was highest for age group < 20 years than for age group 20-49 or 50-80 (e.g. OR = 7.8; 95% CI 2.2-28 for <20 yrs ipsilateral astrocytoma vs OR = 2.1; 95% CI 1.5-2.9 for 20-49 ipsilateral astrocytoma and OR = 1.8; 95% CI 1.3-2.5 for 50-80 ipsilateral astrocytoma. The pattern for cordless phones was similar (OR = 7.9; 95% CI 2.5-25), OR = 1.6; 95% CI 1.1-2.4, and OR = 1.9; 95% CI 1.3-2.7, respectively. No significant risk was found for oligodendroglioma or other/mixed gliomas. For mobile phones and acoustic neuroma, the pattern was similar to astrocytoma (OR =6.8; 95% CI 1.4-34 for < 20 years ipsilateral acoustic neuroma, OR = 2.5; 95% CI 1.6-3.9 for 20-49 yr ipsilateral acoustic neuroma, and OR = 1.1; 95% CI 0.6-1.9 for 50-80 yr ipsilateral acoustic neuroma). For cordless phones and acoustic neuroma the trend was similar to that with mobile phones (OR = 1.7; 95% CI 0.2-16), OR = 2.2; 95% CI 1.4-3.6, and OR = 1.3; 95% CI = 0.7-2.2). Authors' abstract: Hardell et al. 2011: 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. AUTHORS' ABSTRACT: Soderqvist, Carlberg and Hardell 2012 (IEEE #5165):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. AUTHORS' ABSTRACT: Hardell et al. 2012 (IEEE #5217): 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 e10 years (>10 years in the Hardell group) latency group. Ipsilateral mobile phone use e1640h 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 e10 years gave OR=1.81, 95% CI=0.73-4.45. For ipsilateral cumulative use e1640h 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. AUTHORS' ABSTRACT: Hardell et al. 2013 (IEEE #5273): We previously conducted a case-control study of acoustic neuroma. Subjects of both genders aged 20-80 years, diagnosed during 1997-2003 in parts of Sweden, were included, and the results were published. We have since made a further study for the time period 2007-2009 including both men and women aged 18-75 years selected from throughout the country. These new results for acoustic neuroma have not been published to date. Similar methods were used for both study periods. In each, one population-based control, matched on gender and age (within five years), was identified from the Swedish Population Registry. Exposures were assessed by a self-administered questionnaire supplemented by a phone interview. Since the number of acoustic neuroma cases in the new study was low we now present pooled results from both study periods based on 316 participating cases and 3,530 controls. Unconditional logistic regression analysis was performed, adjusting for age, gender, year of diagnosis and socio-economic index (SEI). Use of mobile phones of the analogue type gave odds ratio (OR) = 2.9, 95% confidence interval (CI) = 2.0-4.3, increasing with >20 years latency (time since first exposure) to OR = 7.7, 95% CI = 2.8-21. Digital 2G mobile phone use gave OR = 1.5, 95% CI = 1.1-2.1, increasing with latency >15 years to an OR = 1.8, 95% CI = 0.8-4.2. The results for cordless phone use were OR = 1.5, 95% CI = 1.1-2.1, and, for latency of >20 years, OR = 6.5, 95% CI = 1.7-26. Digital type wireless phones (2G and 3G mobile phones and cordless phones) gave OR = 1.5, 95% CI = 1.1-2.0 increasing to OR = 8.1, 95% CI = 2.0-32 with latency >20 years. For total wireless phone use, the highest risk was calculated for the longest latency time >20 years: OR = 4.4, 95% CI = 2.2-9.0. Several of the calculations in the long latency category were based on low numbers of exposed cases. Ipsilateral use resulted in a higher risk than contralateral for both mobile and cordless phones. OR increased per 100 h cumulative use and per year of latency for mobile phones and cordless phones, though the increase was not statistically significant for cordless phones. The percentage tumour volume increased per year of latency and per 100 h of cumulative use, statistically significant for analogue phones. This study confirmed previous results demonstrating an association between mobile and cordless phone use and acoustic neuroma. AUTHORS' ABSTRACT: Carlberg et al. 2013 (IEEE #5274): BACKGROUND: To study the association between use of wireless phones and meningioma. METHODS:We performed a case--control study on brain tumour cases of both genders aged 18--75 years and diagnosed during 2007--2009. One population-based control matched on gender and age was used to each case. Here we report on meningioma cases including all available controls. Exposures were assessed by a questionnaire. Unconditional logistic regression analysis was performed. RESULTS: In total 709 meningioma cases and 1,368 control subjects answered the questionnaire. Mobile phone use in total produced odds ratio (OR) = 1.0, 95% confidence interval (CI) = 0.7-1.4 and cordless phone use gave OR = 1.1, 95% CI = 0.8-1.5. The risk increased statistically significant per 100 h of cumulative use and highest OR was found in the fourth quartile (>2,376 hours) of cumulative use for all studied phone types. There was no statistically significant increased risk for ipsilateral mobile or cordless phone use, for meningioma in the temporal lobe or per year of latency. Tumour volume was not related to latency or cumulative use in hours of wireless phones. CONCLUSIONS:No conclusive evidence of an association between use of mobile and cordless phones and meningioma was found. An indication of increased risk was seen in the group with highest cumulative use but was not supported by statistically significant increasing risk with latency. Results for even longer latency periods of wireless phone use than in this study are desirable. AUTHORS' ABSTRACT: Hardell et al. 2013 (IEEE #5312). Previous studies have shown a consistent association between long-term use of mobile and cordless phones and glioma and acoustic neuroma, but not for meningioma. When used these phones emit radiofrequency electromagnetic fields (RF-EMFs) and the brain is the main target organ for the handheld phone. The International Agency for Research on Cancer (IARC) classified in May, 2011 RF-EMF as a group 2B, i.e. a 'possible' human carcinogen. The aim of this study was to further explore the relationship between especially long-term (>10 years) use of wireless phones and the development of malignant brain tumours. We conducted a new case-control study of brain tumour cases of both genders aged 18-75 years and diagnosed during 2007-2009. One population-based control matched on gender and age (within 5 years) was used to each case. Here, we report on malignant cases including all available controls. Exposures on e.g. use of mobile phones and cordless phones were assessed by a self-administered questionnaire. Unconditional logistic regression analysis was performed, adjusting for age, gender, year of diagnosis and socio-economic index using the whole control sample. Of the cases with a malignant brain tumour, 87% (n=593) participated, and 85% (n=1,368) of controls in the whole study answered the questionnaire. The odds ratio (OR) for mobile phone use of the analogue type was 1.8, 95% confidence interval (CI)=1.043.3, increasing with >25 years of latency (time since first exposure) to an OR=3.3, 95% CI=1.6-6.9. Digital 2G mobile phone use rendered an OR=1.6, 95% CI=0.996-2.7, increasing with latency >15-20 years to an OR=2.1, 95% CI=1.2-3.6. The results for cordless phone use were OR=1.7, 95% CI=1.1-2.9, and, for latency of 15-20 years, the OR=2.1, 95% CI=1.2-3.8. Few participants had used a cordless phone for >20-25 years. Digital type of wireless phones (2G and 3G mobile phones, cordless phones) gave increased risk with latency >1-5 years, then a lower risk in the following latency groups, but again increasing risk with latency >15-20 years. Ipsilateral use resulted in a higher risk than contralateral mobile and cordless phone use. Higher ORs were calculated for tumours in the temporal and overlapping lobes. Using the meningioma cases in the same study as reference entity gave somewhat higher ORs indicating that the results were unlikely to be explained by recall or observational bias. This study confirmed previous results of an association between mobile and cordless phone use and malignant brain tumours. These findings provide support for the hypothesis that RF-EMFs play a role both in the initiation and promotion stages of carcinogenesis. AUTHORS' ABSTRACT: Hardell and Carlberg 2013 (IEEE #5388): 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. Methods: 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. Results: 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. Conclusion: 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. AUTHORS' ABSTRACT: Hardell and Carlberg 2013 (IEEE #5477). BACKGROUND: We analysed the survival of patients after glioma diagnosis in relation to the use of wireless phones. METHODS: All cases diagnosed between 1997 and 2003 with a malignant brain tumour (n = 1,251) in our case-control studies were included and followed from the date of diagnosis to the date of death or until May 30, 2012. RESULTS: For glioma, the use of wireless phones (mobile and cordless phones) gave a hazard ratio (HR) = 1.1 (95% confidence interval, CI = 0.9-1.2), with > 10-year latency HR = 1.2 (95% CI = 1.002-1.5, p trend = 0.02). For astrocytoma grade I-II (low-grade), the results were, HR = 0.5 (95% CI = 0.3-0.9) and for astrocytoma grade IV (glioblastoma), HR = 1.1 (95% CI = 0.95-1.4), with > 10 year latency HR = 1.3 (95% CI = 1.03-1.7). In the highest tertile (> 426 h) of cumulative use, HR = 1.2 (95% CI = 0.95-1.5) was found for glioblastoma. The results were similar for mobile and cordless phones. CONCLUSIONS: Decreased survival of glioma cases with long-term and high cumulative use of wireless phones was found. A survival disadvantage for astrocytoma grade IV, but a survival benefit for astrocytoma grade I-II was observed which could be due to exposure-related tumour symptoms leading to earlier diagnosis and surgery in that patient group. AUTHORS' ABSTRACT: Soderqvist et al. 2011 (IEEE #5652): Case-control studies on adults point to an increased risk of brain tumours (glioma and acoustic neuroma) associated with the long-term use of mobile phones. Recently, the first study on mobile phone use and the risk of brain tumours in children and adolescents, CEFALO, was published. It has been claimed that this relatively small study yielded reassuring results of no increased risk. We do not agree. We consider that the data contain several indications of increased risk, despite low exposure, short latency period, and limitations in the study design, analyses and interpretation. The information certainly cannot be used as reassuring evidence against an association, for reasons that we discuss in this commentary. AUTHORS' ABSTRACT: Hardell and Carlberg 2014 (IEEE #5803): We made a pooled analysis of two case-control studies on malignant brain tumours with patients diagnosed during 19972003 and20072009. They were aged 2080 years and 1875 years, respectively, at the time of diagnosis. Only cases with histopathological verification of the tumour were included. Population-based controls, matched on age and gender, were used. Exposures were assessed by questionnaire. The whole reference group was used in the unconditional regression analysis adjusted for gender, age, year of diagnosis, and socio-economic index. In total, 1498 (89%) cases and 3530 (87%) controls participated. Mobile phone use increased the risk of glioma, OR = 1.3, 95%CI = 1.11.6 overall, increasing to OR = 3.0, 95% CI = 1.75.2 in the >25 year latency group. Use of cordless phones increased the risk to OR = 1.4, 95% CI = 1.11.7, with highest risk in the >1520 years latency group yielding OR = 1.7, 95% CI = 1.12.5. The OR increased statistically significant both per 100 h of cumulative use, and per year of latency for mobile and cordless phone use. Highest ORs overall were found for ipsilateral mobile or cordless phone use, OR = 1.8, 95% CI = 1.42.2 and OR = 1.7, 95% CI = 1.32.1, respectively. The highest risk was found for glioma in the temporal lobe. First use of mobile or cordless phone before the age of 20 gave higher OR for glioma than in later age groups. AUTHORS' ABSTRACT: Carlberg and Hardell 2014 (IEEE #5849): On 31 May 2011 the WHO International Agency for Research on Cancer (IARC) categorised radiofrequency electromagnetic fields (RF-EMFs) from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields, as a Group 2B, i.e., a possible , human carcinogen. A causal association would be strengthened if it could be shown that the use of wireless phones has an impact on the survival of glioma patients. We analysed survival of 1678 glioma patients in our 19972003 and 20072009 case-control studies. Use of wireless phones in the >20 years latency group (time since first use) yielded an increased hazard ratio (HR) = 1.7, 95% confidence interval (CI) = 1.22.3 for glioma. For astrocytoma grade IV (glioblastoma multiforme; n = 926) mobile phone use yielded HR = 2.0, 95% CI = 1.42.9 and cordless phone use HR = 3.4, 95% CI = 1.0411 in the same latency category. The hazard ratio for astrocytoma grade IV increased statistically significant per year of latency for wireless phones, HR = 1.020, 95% CI = 1.0071.033, but not per 100 h cumulative use, HR = 1.002, 95% CI = 0.9991.005. HR was not statistically significant increased for other types of glioma. Due to the relationship with survival the classification of IARC is strengthened and RF-EMF should be regarded as human carcinogen requiring urgent revision of current exposure guidelines. AUTHORS' ABSTRACT: Hardell and Carlberg 2015 (IEEE #5850): We made a pooled analysis of two case-control studies on malignant brain tumours with patients diagnosed during 19972003 and 20072009. They were aged 2080 years and 1875 years, respectively, at the time of diagnosis. Only cases with histopathological verification of the tumour were included. Population-based controls, matched on age and gender, were used. Exposures were assessed by questionnaire. The whole reference group was used in the unconditional regression analysis adjusted for gender, age, year of diagnosis, and socio-economic index. In total, 1498 (89%) cases and 3530 (87%) controls participated. Mobile phone use increased the risk of glioma, OR=1.3, 95% CI=1.11.6 overall, increasing to OR=3.0, 95% CI=1.75.2 in the >25 year lat |
|
| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | Regional Hospital, Orebro, Sweden - lennart.hardell@orebroll.se | |
| Funding Agency | ????? | |
| Country | SWEDEN | |
| References |
|
|
| Comments | INSERT in SUMMARY: OR = 2.6; 95% CI 1.5-4.3 glioma/analog OR = 1.9; 95% CI 1.3-2.7 glioma/digital OR = 2.1; 95% CI 1.4-3.0 glioma/cordless OR = 2.1; 95% CI=1.5-2.9 glioma/ipsilateral analog OR = 1.8; 95% CI 1.4-2.4 glioma/ipsilateral digital OR = 1.7; 95% CI 1.3-2.2 glioma/ipsilateral cordless OR = 2.7; 95% CI 1.8-4.2 glioma/10+ yr analog OR = 3.8; 95% CI 1.8-8.1 glioma/10+ yr digital OR = 2.2; 95% CI 1.3-3.9 glioma/10+ yr cordless OR = 0.92; 95% CI 0.58-1.44 parotid/analog OR = 1.01; 95% CI 0.68-1.50 parotid/digital OR = 0.99; 95% CI 0.68-1.43 parotid/cordless OR = 2.0; 95% CI 1.1-3.8 AN/analog OR = 1.4; 95% CI 0.8-2.4 AN/digital OR = 4.2; 95% CI 1.8-10 AN/10+ yr analog OR = 2.0; 95% CI 1.05-3.8 AN/10+ yr digital OR = 1.7 ; 95% CI 0.97 3.0 meningioma/analog OR = 1.3 ; 95% CI 0.9-1.9 meningioma/digital OR = 2.1; 95% CI = 1.1-4.3 meningioma/10+ yr analog Notes: "Cases" in initial studies were defined as users having between 8 hrs and 9000 hrs total cumulative time, and for laterality comparisons in the initial study, users had between 16 and 1064 total cumulative hours of phone use, with most of the 13 individuals having less than 250 hours total. Exposure assessment in later studies, especially information on laterality, phone type, and mean number and length of calls, was also questionnaire-based supplimented by telephone interview and not fully described – with possible recall inaccuracy and recall bias. Regarding tumor location, it was not clear that the anatomical location in all the reported 1358 patients was verified by radiology reports. The results are not supported by laterality or total tumor data from Muscat et al (1999), Inskip et al (2000), Johanson et al (2001), or Auvinen (2002). In the 2002 studies, Hardell grouped both benign and malignant tumors together for statistical analysis, which he did not do for the earlier studies (1999), and reported a correlation between NMT and total tumors that was basically a function of the benign tumor contribution – there was no correlation with malignant tumors alone in previous studies, although in the 2003 Int J Oncology report there was a correlation between NMT use and ipsilateral astrocytoma. In contrast, Auvinen 2002 reported no association with benign tumors, but a slight association with malignant gliomas. In the 2002 studies, cases and controls were matched on age, sex, and residential location. In the Int J Oncology 2003 study, cases and controls were not matched, but assigned to exposed or unexposed categories according to phone type (with adjustment for age, gender, and SES), representing an alternative analysis of the same data, although similar results obtained (some variations in the tumor vs. exposure numbers can be seen by comparing Table 2 of Hardell et al., 2002 vs. Table II of Hardell et al., Int J Oncology 2003). Interestingly, the 2002 study did show an apparent dose response using univariate analysis, although multivariate analysis (Table 7) showed a statistical association only with NMT use for > 1 year, and not with >5 year and >10 year exposure groups. Of 262 cases identified, 209 (80%) are in the study were used for study analysis but only 198 (76%) are included in the detailed tables. In the statistical analysis, original numbers were rounded up, but not rounded down (for example, OR 1.26, 95% CI 1.02-1.56 became OR1.3, CI 1.02 - 1.6). All studies were restricted to subjects alive at the time of the study, possibly excluding more aggressive tumor types in the analysis. The finding of no association with salivary gland tumors agrees with a similar finding by Auvinen et al (Epidemiology (2002) 13:356-359) that reported an OR 1.3, 95% CI 0.4 - 4.7 for salivary gland tumors. In the recent 2006 paper, the Discussion references Christensen et al Am J Epidemiol (2004) 159:277-283 as supporting an increase in AN. This is incorrect (Christensen 2004 states no increase in AN, and Christensen 2005 reports a decrease in high grade AN, although Lonn et al Epidemiology (2005)161:526-535) did reporte increased ipsilateral AN incidence in long term users (maybe just a mistaken reference ?). For the meta-analysis (2007), no description was provided for how the meta-analysis was performed. Kelsh and Erdrich did a meta-analysis on the same populations that Hardell did his meta-analysis on in 2007, 2008 papers. Kelsh et al note the following: 1) Double counting by Hardell et al. In the meta-analysis Hardell et al included individual studies as well as the studies that pooled these individual studies together, thus counting several populations twice. Kelsh et al removed the duplicate study populations 2) Latency versus duration Latency is defined as time since first use, which could include durations of use from 6 months to 10 years. Hardell et al based his analysis on latency and did not analyze duration of use. The analysis by Kelsh et al , evaluated duration of use for >10 years in addition to latency >10 years. The meta-analyses by Kelsh et al for duration >10 years did not show elevated risks or statistically significant risks for any of the tumors. Kelsh et al also notes that latency from use to tumor development could take longer than 10 years, thus current studies may not yet be long enough. 3) Hardell did find results showing no association, but his reporting emphasizes the associations. Hardell et al found statistically significant results for a few analyses: Ipsilateral use for gliomas and acoustic neuromas for latency of use >10 years. The remaining analyses by Hardell et al were not elevated or statistically significant, however he gives minimal attention to those results. 4) Differences in Ipsilateral associations Kelsh et al removed duplicate studies from the analysis of Ipsilateral use with latency >10 years and did not find a statistically significant association. Compared to Hardell et al, Kelsh et al only included 2 studies for each analysis by tumor for latency >10 years compared to 3 or 4 by Hardell due to the double counting described above. . 5) Ipsilateral versus contralateral use Hardell et al does not discuss the difference observed between the increased risks for ipsilateral use versus no observed risk for contralateral use. Limitations to the analysis of ipsilateral and contralateral use include differential recall with cases recalling the side of use as same side as tumor more often than controls. Lonn et al (2005) gathered his data from regional cancer registries in Umea, Stockholm, Goeteborg, and Lund from September 1, 2000 thorugh August 31, 2002, while Hardell et al (2002, 2005,2006) gathered data from registries in Uppsala-Orebro, Stockholm, Linkoping, and Goteborg from January 1997 through June 2000 and extended through December 2003. Since much of this data overlaps, it is odd that such different ORs were obtained. That point could be emphasized. |