RE: "CELLULAR TELEPHONE USE AND RISK OF ACOUSTIC NEUROMA"

Michael Kundi

Institute of Environmental Health, Medical University of Vienna, 1095 Vienna, Austria

In their recent article reporting results of a Danish case-control study of acoustic neuroma, Christensen et al. concluded "that there is no evidence for an association between use of cellular telephones and the risk of developing acoustic neuroma" (1, p. 282). This conclusion is not in line with the study hypothesis. The authors stated that the biologic basis for an association between cell phone use and cancer could be a thermal or nonthermal mechanism that promotes tumor growth. This, of course, extends to benign tumors such as acoustic neuroma. Indeed, there is up to now no solid basis for the assumption of a tumor-initiating capacity of microwaves and, in particular, of mobile phone use. Concerning acoustic neuroma, long induction periods and latencies have been indicated (2, 3). There are diverse patterns of schwannoma growth (4), the reason for which is largely unknown. Average volume doubling times of about 2 years were found (5). Considering this evidence, what can be expected as the result of a case-control study of a factor possibly promoting tumor growth? First of all, as the authors correctly stated, exposure to microwaves from mobile phone use is restricted to the side of the head where the telephone is held during telephoning. Hence, only in subjects that used the telephone on the same side of the head as the tumor is located can an effect on tumor growth be expected. However, unilateral hearing loss and tinnitus are likely to interfere with this habit if the tumor happens to be located on the side of predominant use. There are several indications in the data presented that such symptoms changed usage pattern: 20 percent of cellular telephone users among cases compared with 6 percent in controls had no preferred side of telephone use, ipsilateral use was significantly less frequent, and there was a decrease of odds ratios by the time since first use and cumulative number of calls. These data suggest that the growing tumor led to a reduction in or even cessation of phone use and to switching side of the head in response to hearing loss. Similar results have been obtained previously (6). On the other hand, the mean size of the tumors in mobile phone users was significantly greater (1.66 cm3) than in nonusers (1.39 cm3). Considering an average annual tumor growth of 0.1 cm3 and an average duration of mobile phone use of about 3.5 years, this difference is consistent with a substantial increase of growth rate. Combining these lines of evidence, the data presented so far are insufficient to decide about a promoter effect of mobile phone use. Analysis has to consider the influence of symptoms on mobile phone use and laterality. However, it seems that there are too few cases of long-term use to make such an analysis meaningful.

Furthermore, it must be stressed that odds ratios considerably underestimate the effects on tumor growth. The predominant effect of a promoter is a shift of the distribution of age at diagnosis by a fraction of exposure duration. If exposure duration is short relative to the natural history of the disease and the age-incidence function has a flat slope, the odds ratios from age-matched case-control studies are generally too low to indicate an effect even if the agent under study does substantially increase the tumor growth rate.

Future publications of results obtained within the framework of the Interphone Study of the World Health Organization should probably avoid presenting analyses that are based on the assumption of a tumor-inducing capacity of emissions from mobile phones, because 1) the vast majority of brain tumors have induction periods and latencies that typically exceed exposure duration that could have been accumulated up to now, and 2) promoting effects will be obscured.

REFERENCES

REFERENCES

  1. Christensen HC, Schüz J, Kosteljanetz M, et al. Cellular telephone use and risk of acoustic neuroma. Am J Epidemiol 2004;159:277–83.[Abstract/Free Full Text]
  2. Anderson TD, Loevner LA, Bigelow DC, et al. Prevalence of unsuspected acoustic neuroma found by magnetic resonance imaging. Otolaryngol Head Neck Surg 2000;122:643–6.[ISI][Medline]
  3. Rosenberg SI. Natural history of acoustic neuromas. Laryngoscope 2000;110:497–508.[CrossRef][ISI][Medline]
  4. Mohyuddin A, Vokurka EA, Evans DGR, et al. Is clinical growth index a reliable predictor of tumour growth in vestibular schwannomas? Clin Otolaryngol 2003;28:85–90.[ISI][Medline]
  5. Steinhart H, Triebswetter F, Wolf S, et al. Growth of sporadic vestibular schwannomas correlates with Ki-67 proliferation index. (In German). Laryngorhinootologie 2003;82:318–21.[CrossRef][Medline]
  6. Muscat JE, Malkin MG, Shore RE, et al. Handheld cellular telephones and risk of acoustic neuroma. Neurology 2002;58:1304–6.[Abstract/Free Full Text]