The increased use of radiofrequency (RF) fields above 6 GHz, particularly for the 5 G mobile phone network, has given rise to public concern about any possible adverse effects to human health. Public exposure to RF fields from 5 G and other sources is below the human exposure limits specified by the International Commission on Non-Ionizing Radiation Protection (ICNIRP). This state-of-the science review examined the research into the biological and health effects of RF fields above 6 GHz at exposure levels below the ICNIRP occupational limits. The review included 107 experimental studies that investigated various bioeffects including genotoxicity, cell proliferation, gene expression, cell signalling, membrane function and other effects. Reported bioeffects were generally not independently replicated and the majority of the studies employed low quality methods of exposure assessment and control. Effects due to heating from high RF energy deposition cannot be excluded from many of the results. The review also included 31 epidemiological studies that investigated exposure to radar, which uses RF fields above 6 GHz similar to 5 G. The epidemiological studies showed little evidence of health effects including cancer at different sites, effects on reproduction and other diseases. This review showed no confirmed evidence that low-level RF fields above 6 GHz such as those used by the 5 G network are hazardous to human health. Future experimental studies should improve the experimental design with particular attention to dosimetry and temperature control. Future epidemiological studies should continue to monitor long-term health effects in the population related to wireless telecommunications.

The objective of this review was to assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to radiofrequency electromagnetic fields (RF-EMF) and risk of the most investigated neoplastic diseases. Eligibility criteria: We included cohort and case-control studies of neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of hand-held transceivers or RF-emitting equipment in the workplace (SR-C). While no restrictions on tumour type were applied, in the current paper we focus on incidence-based studies of selected "critical" neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). We focussed on investigations of specific neoplasms in relation to specific exposure sources (i.e. E-O pairs), noting that a single article may address multiple E-O pairs. Eligible studies were identified by literature searches through Medline, Embase, and EMF-Portal. Risk-of-bias (RoB) assessment: We used a tailored version of the Office of Health Assessment and Translation (OHAT) RoB tool to evaluate each study's internal validity. At the summary RoB step, studies were classified into three tiers according to their overall potential for bias (low, moderate and high). We synthesized the study results using random effects restricted maximum likelihood (REML) models (overall and subgroup meta-analyses of dichotomous and categorical exposure variables), and weighted mixed effects models (dose-response meta-analyses of lifetime exposure intensity). Evidence assessment: Confidence in evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. We included 63 aetiological articles, published between 1994 and 2022, with participants from 22 countries, reporting on 119 different E-O pairs. RF-EMF exposure from mobile phones (ever or regular use vs no or non-regular use) was not associated with an increased risk of glioma [meta-estimate of the relative risk (mRR) = 1.01, 95 % CI = 0.89-1.13), meningioma (mRR = 0.92, 95 % CI = 0.82-1.02), acoustic neuroma (mRR = 1.03, 95 % CI = 0.85-1.24), pituitary tumours (mRR = 0.81, 95 % CI = 0.61-1.06), salivary gland tumours (mRR = 0.91, 95 % CI = 0.78-1.06), or paediatric (children, adolescents and young adults) brain tumours (mRR = 1.06, 95 % CI = 0.74-1.51), with variable degree of across-study heterogeneity (I² = 0 %-62 %). There was no observable increase in mRRs for the most investigated neoplasms (glioma, meningioma, and acoustic neuroma) with increasing time since start (TSS) use of mobile phones, cumulative call time (CCT), or cumulative number of calls (CNC). Cordless phone use was not significantly associated with risks of glioma [mRR = 1.04, 95 % CI = 0.74-1.46; I² = 74 %) meningioma, (mRR = 0.91, 95 % CI = 0.70-1.18; I² = 59 %), or acoustic neuroma (mRR = 1.16; 95 % CI = 0.83-1.61; I² = 63 %). Exposure from fixed-site transmitters (broadcasting antennas or base stations) was not associated with childhood leukaemia or paediatric brain tumour risks, independently of the level of the modelled RF exposure. Glioma risk was not significantly increased following occupational RF exposure (ever vs never), and no differences were detected between increasing categories of modelled cumulative exposure levels. In the sensitivity analyses of glioma, meningioma, and acoustic neuroma risks in relation to mobile phone use (ever use, TSS, CCT, and CNC) the presented results were robust and not affected by changes in study aggregation. In a leave-one-out meta-analyses of glioma risk in relation to mobile phone use we identified one influential study. In subsequent meta-analyses performed after excluding this study, we observed a substantial reduction in the mRR and the heterogeneity between studies, for both the contrast Ever vs Never (regular) use (mRR = 0.96, 95 % CI = 0.87-1.07, I² = 47 %), and in the analysis by increasing categories of TSS (" 1.5 with a 10+ years induction period were definitely implausible, and could be used to set a "credibility benchmark". In the sensitivity meta-analyses of glioma risk in the upper category of TSS excluding five studies reporting implausible effect sizes, we observed strong reductions in both the mRR [mRR of 0.95 (95 % CI = 0.86-1.05)], and the degree of heterogeneity across studies (I² = 3.6 %). Consistently with the published protocol, our final conclusions were formulated separately for each exposure-outcome combination, and primarily based on the line of evidence with the highest confidence, taking into account the ranking of RF sources by exposure level as inferred from dosimetric studies, and the external coherence with findings from time-trend simulation studies (limited to glioma in relation to mobile phone use). For near field RF-EMF exposure to the head from mobile phone use, there was moderate certainty evidence that it likely does not increase the risk of glioma, meningioma, acoustic neuroma, pituitary tumours, and salivary gland tumours in adults, or of paediatric brain tumours. For near field RF-EMF exposure to the head from cordless phone use, there was low certainty evidence that it may not increase the risk of glioma, meningioma or acoustic neuroma. For whole-body far-field RF-EMF exposure from fixed-site transmitters (broadcasting antennas or base stations), there was moderate certainty evidence that it likely does not increase childhood leukaemia risk and low certainty evidence that it may not increase the risk of paediatric brain tumours. There were no studies eligible for inclusion investigating RF-EMF exposure from fixed-site transmitters and critical tumours in adults. For occupational RF-EMF exposure, there was low certainty evidence that it may not increase the risk of brain cancer/glioma, but there were no included studies of leukemias (the second critical outcome in SR-C). The evidence rating regarding paediatric brain tumours in relation to environmental RF exposure from fixed-site transmitters should be interpreted with caution, due to the small number of studies. Similar interpretative cautions apply to the evidence rating of the relation between glioma/brain cancer and occupational RF exposure, due to differences in exposure sources and metrics across the few included studies. This project was commissioned and partially funded by the World Health Organization (WHO). Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; and ARPANSA as a WHO Collaborating Centre for Radiation Protection. PROSPERO CRD42021236798. Published protocol: [(Lagorio et al., 2021) DOI https://doi.org/10.1016/j.envint.2021.106828].

The World Health Organization (WHO) has an ongoing project to assess potential health effects of exposure to radiofrequency electromagnetic fields (RF-EMF) in the general and working population. Here we present the protocol for a systematic review of the scientific literature on cancer hazards from exposure to RF-EMF in humans, commissioned by the WHO as part of that project. To assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to RF-EMF and risk of neoplastic diseases. We will include cohort and case-control studies investigating neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of handheld transceivers or RF-emitting equipment in the workplace (SR-C). While no restriction on tumour type will be applied, we will focus on selected neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). Eligible studies will be identified through Medline, Embase, and EMF-Portal. We will use a tailored version of the OHAT's tool to evaluate the study's internal validity. We will consider separately studies on different tumours, neoplasm-specific risks from different exposure sources, and a given exposure-outcome pair in adults and children. When a quantitative synthesis of findings can be envisaged, the main aims of the meta-analysis will be to assess the strength of association and the shape of the exposure–response relationship; to quantify the degree of heterogeneity across studies; and explore the sources of inconsistency (if any). When a meta-analysis is judged inappropriate, we will perform a narrative synthesis, complemented by a structured tabulation of results and appropriate visual displays. Confidence in evidence will be assessed in line with the GRADE approach. This project is supported by the World Health Organization. Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; ARPANSA as a WHO Collaborating Centre for Radiation Protection. PROSPERO CRD42021236798.

Objective Some studies have reported increasing trends in certain brain tumours and a possible link with mobile phone use has been suggested. We examined the incidence time trends of brain tumour in Australia for three distinct time periods to ascertain the influence of improved diagnostic technologies and increase in mobile phone use on the incidence of brain tumours. Design In a population-based ecological study, we examined trends of brain tumour over the periods 1982–1992, 1993–2002 and 2003–2013. We further compared the observed incidence during the period of substantial mobile phone use (2003–2013) with predicted (modelled) incidence for the same period by applying various relative risks, latency periods and mobile phone use scenarios. Setting National Australian incidence registration data on primary cancers of the brain diagnosed between 1982 and 2013. Population 16 825 eligible brain cancer cases aged 20–59 from all of Australia (10 083 males and 6742 females). Main outcome measures Annual percentage change (APC) in brain tumour incidence based on Poisson regression analysis. Results The overall brain tumour rates remained stable during all three periods. There was an increase in glioblastoma during 1993–2002 (APC 2.3, 95% CI 0.8 to 3.7) which was likely due to advances in the use of MRI during that period. There were no increases in any brain tumour types, including glioma (−0.6, –1.4 to 0.2) and glioblastoma (0.8, –0.4 to 2.0), during the period of substantial mobile phone use from 2003 to 2013. During that period, there was also no increase in glioma of the temporal lobe (0.5, –1.3 to 2.3), which is the location most exposed when using a mobile phone. Predicted incidence rates were higher than the observed rates for latency periods up to 15 years. Conclusions In Australia, there has been no increase in any brain tumour histological type or glioma location that can be attributed to mobile phones.

Background Although the aetiology of glioma is poorly understood, the higher incidence in males has long suggested an occupational cause.

Background: With the roll-out of new technologies such as 5G, there has been renewed community concern regarding the adequacy of research on possible health effects from associated radiofrequency radiation, mainly in the millimetre wave (MMW) band. Objective: We conducted a meta-analysis of in vitro and in vivo studies investigating bioeffects of MMWs at low exposure levels. Methods: We identified 107 in vitro and in vivo studies investigating MMWs and biological effects in which the power density employed has been below 100 W/m², which is below the current standards for occupational local exposures. Where possible, we estimated the magnitude of the principal effect reported or set this magnitude to zero in studies reporting no significant effects. We also estimated the quality of the studies, based on a methodology used in previous analyses. Results: We show a negative correlation between effect size and both power density and specific absorption rate. There was also a significant negative correlation between effect size and quality score. A multivariate analysis revealed that there is an increase in the effect size for certain biological systems being investigated and laboratories in which the work was carried out whilst the quality score for some of these tends to be low. We note that many of the studies were motivated by a desire to elucidate the possible mechanisms in therapeutic devices rather than assessing the safety of telecommunications systems. Finally, it appears that the presence or absence of modulation does not influence the reported effect size. Significance: Many of the findings of this meta-analysis have not been reported before and have important implications for overall interpretation of in vitro and in vivo data. Overall, the results of this study do not confirm an association between low-level MMWs and biological effects.