The carcinogenic effect of radiofrequency electromagnetic fields (RF-EMF) on humans was evaluated at a meeting during 24 – 31 May 2011 at the International Agency for Research on Cancer (IARC) at WHO in Lyon, France. The Working Group categorised RF-EMF from mobile phones, and from other devices that emit similar non-ionising electromagnetic fields, as a Group 2B, i.e. a ‘possible’, human carcinogen.
After that meeting supportive evidence has come from e.g. the French CERENAT study and also our recent publication on glioma. An increased risk for acoustic neuroma associated with use of wireless phones was published by our research group after the meeting giving pooled results of our study periods 1997-2003 and 2007-2009. Also other studies have reported similar findings.
We evaluated the Hill viewpoints on association and causation used in the 1960’s in the debate on lung cancer risk among smokers. Using these viewpoints our summary was that RF-EMF exposure should be a Group 1 carcinogen according to IARC criteria. There is now a petition to support that notion aiming at alerting IARC to classify such exposure to cause human cancer. Those who want to support the petition can follow this link.
We published recently a pooled analysis of our case-control studies on glioma and use of mobile phones and cordless phones. The study has been published in Pathophysiology after pre-review and can be accessed via Internet. The results confirm a statistically significant increased risk for glioma and the risk increases with time from first use of the wireless phone and number of hours for use over the years. The risk is highest on the same side of the brain as the phone has been used, especially in the area with the highest exposure to microwaves, the temporal lobe, which would be expected.
These studies strengthen the 2011 classification by IARC at WHO that the microwave exposure is a ‘Possible human carcinogen’, Group 2B. In fact using the Hill viewpoints on association and causation it should be classified as Group 1, the agent causes human cancer. We have explored that fact in more detail in a previous article. The present results confirm that classification.
Our results have gained interest in many countries after a press release by Reuters and have also been discussed in the Finnish Medical newspaper. However, these worrying results for human health have not been discussed at all in Sweden, so the layman is uniformed about how important it is to avoid such exposure.
In a new study a decreased survival was found in glioblastoma patients with long-term use of mobile and cordless phones. The study is free to download here.
According to the study 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) = 1.2–2.3 for glioma, a decreased survival. For astrocytoma grade IV (glioblastoma multiforme; n = 926) mobile phone use yielded HR = 2.0, 95% CI = 1.4–2.9 and cordless phone use HR = 3.4, 95% CI = 1.04–11 in the same latency category. Due to the relationship with survival the classification of IARC (possibly carcinogenic to humans, Group 2B) is strengthened and RF-EMF should be regarded as human carcinogen requiring urgent revision of current exposure guidelines. The findings are discussed in detail in the article.
The p53 protein is a transcription factor that plays a vital role in regulating cell growth, DNA repair and apoptosis, and p53 mutations are involved in disease progression. In a recent study it was found that use of mobile phones for ≥3 hours a day was associated with increased risk for the mutant type of p53 gene expression in the peripheral zone of astrocytoma grade IV. The mutation was statistically significant correlated with shorter overall survival time. The study was rather small (n=63) and no data on latency of mobile phone use was given.
We have previously reported decreased survival in patients with glioblastoma multiforme associated with use of mobile phones. The present study supports our findings and gives insight into a possible genetic mechanism both for the increased risk for glioblastoma multiforme and the decreased survival.