Swerdlow et al. next heaviest decile of users it was 0.76 (95% CI: 0.54, 1.08). Furthermore, the top decile category presented was not actually 10% of the control data—it is unknown to what extent risk would have been raised in the true top decile, or to what extent the raised risk is a function of the cut-point chosen (about the 7th percentile for meningioma and the 8th percentile for glioma). The only previously available risk estimates among comparably heavy users are from case– control studies conducted by Hardell et al. (2006a, 2006b) in Sweden, which reported a markedly raised risk and positive dose– response gradient for “malignant tumors” but not for meningioma. We have discussed elsewhere why the Hardell et al. results are problematic (Ahlbom et al. 2009). Assessment of the findings with respect to cumulative call time in individual published component studies of Interphone, whose participants variously covered a wider range of ages than Interphone, confirmed the lack of dose– response effect with glioma [see Supplemental Material, p. 2 (http://dx.doi.org/10.1289/ ehp.1103693)]. Furthermore, for number of calls, which validation studies suggest may be better reported than cumulative hours of exposure, there was no indication of raised risk in the top decile or of dose response. Finally, participants who had been using mobile phones the longest (≥ 10 years) and had accumulated highest lifetime call hours (≥ 1,640 hr) might be expected a priori to have been at the highest risk if RF exposure were tumorigenic. This was not the case, however, for either glioma (OR = 1.34; 95% CI: 0.90, 2.01) or meningioma (OR = 0.95; 95% CI: 0.56, 1.63) (Interphone Study Group 2010). Instead, it appeared that the very few individuals who started regular use only 1–4 years ago yet whose cumulative call time fell in the highest decile, because of their reported recent heavy use, carried the greatest risk of both tumor types: for glioma OR = 3.77 (95% CI: 1.25, 11.4) and for menin- gioma OR = 4.80 (95% CI: 1.49, 15.4), with no dose response. The similarity of the results for meningioma and glioma suggests that shared recall bias exists, because such a recent use period should have little or no bearing on the pathogenesis of meningioma, which tends to have a long latent period. The magnitudes of relative risk of glioma and meningioma found in the top decile of cumulative use of phones were not large (1.40 and 1.15, respectively) and are on the margins of what epidemiology can detect. It is at a level at which the errors and biases identified in the study data provide a plausible—in- deed, at present a more plausible—alternative explanation of the findings than does causa- tion. Furthermore, the analyses were derived from a very large number of comparisons 1536 investigated [some reported by the Interphone Study Group (2010), the great majority not]; hence, there was the potential for selective emphasis in presentation of the results. In summary, the Interphone study and the literature overall have methodological deficiencies but do not demonstrate greater risk of either glioma or meningioma with lon- ger or greater use of mobile phones, although the longest period since first use examined is < 15 years. Anatomic Distribution of the Tumors Compared with Anatomic Distribution of Exposure RF exposure during mobile phone use is highly attenuated within a few centimeters in the brain, so exposure is largely to the side of the brain, and to the anatomic area, closest to the antenna. It has been reported that on the side of the brain where the phone is used, 50–60% of the total RF energy is absorbed in the temporal lobe, and the average specific absorption rate is highest in the temporal lobe and the cerebellum (Cardis et al. 2008). Thus, examination of location of the tumor in rela- tion to location of exposure is of interest. Laterality. If there were a causal associa- tion between mobile phone use and brain tumor risk, one would expect an increased risk on the same side of the head as the phone is held and a finding on the opposite side. On the other hand, if some brain tumor patients believed that mobile phone use had caused their tumor, and consequently over- reported use on the affected side, this would result in an apparent risk increase on the same side of the head accompanied by a decreased risk on the opposite side. (The same bias is not possible for controls, who do not have a tumor side.) Furthermore, if there were a causal relationship, one would expect an effect of laterality to occur after a sufficient induc- tion period, not for solely recent use (unless there was a promotional effect of mobile phones that was very rapid and substantial, which presumably would be easily and rapidly detectable from population incidence trends). ORs for glioma and meningioma in the Interphone study tended to be greater in sub- jects who reported usual phone use on the same side of the head as their tumor than on the opposite side for most categories of dura- tion of use, cumulative call time, and cumu- lative number of calls. Most ipsilateral ORs were not above unity, however, and there was no dose–response trend, although the great- est ORs tended to be for the top decile of ipsilateral exposure. There are currently no validation studies of retrospective self-reported side of use, and there is no evidence of consistency over time in the preferred side of use. Overall, the greater risk for reported ipsilateral than contralateral use would be compatible with causation or bias as an explanation, but the finding that contral- ateral risks and many of the ipsilateral risks were generally below unity, with no consistent pattern of greater ipsilateral/contralateral ratios with greater exposure (except for cumulative number of calls and risk of glioma), would favor bias as the explanation. Lobe. The risk of glioma in the temporal lobe for regular use and for most categories of exposure was reduced and did not differ from that in other lobes. ORs for long-term use and highest cumulative call time, however, were somewhat greater in the temporal lobe than in other lobes. This is the pattern one would expect if there were a causal effect, although there was no suggestion of a dose–response effect for temporal tumors, which would also be expected if there were causality. No coher- ent pattern was observed for meningioma, for which the OR for temporal lobe tumors for regular use was somewhat lower than for other lobes, and there was no evidence of greater risk in the temporal than other lobes in other categories of use. Exact anatomic location of the tumor. Interphone collected neuroradiologic infor- mation on the exact locations of brain tumors in the study. Although this has not been published for the study overall, it has been published for glioma for many of the study centers and for meningioma for one center. These analyses gave no indication of an associ- ation of tumor risk to proximity of the tumor to the exposure source (Larjavaara et al. 2011; Takebayashi et al. 2008). In summary, among the three types of data on anatomic location, the results for laterality of phone use are the least interpretable. They are compatible with bias, or at least partly with causation, but do not give firm evidence for either. The evidence on lobe of glioma, but not of meningioma, is inconsistently in the direction that would be expected with causal- ity, but not decisively so. The evidence on exact location of the tumor, which one would expect to give the most rigorous analysis because it has greater precision without bias, does not support a causal association. Data on tumor risk in relation to type of mobile phone, and hence of exposure, have not suggested a relation [see Supplemental Material, p. 2 (http://dx.doi.org/10.1289/ ehp.1103693)]. Other Relevant Evidence The biological literature on RF and can- cer does not support an etiologic effect— extensive research has not established any biological mechanism by which RF fields, which are not mutagenic, could cause can- cer, and animal experiments have given no replicable evidence for cancer causation in ovlume 119 | number 11 | November 2011 • Environmental Health Perspectives