DOI: 10.3390/cancers18213419 ISSN: 2072-6694

Ecological Analysis of Spatiotemporal Patterns in Brain Tumor Incidence and Cellular Infrastructure Growth in the United States

János A. Barbero, Prashin Unadkat, Daniel G. Eichberg, Randy S. D’Amico, Daniel M. Sciubba, Michael Schulder, Jung Park

Background/Objectives: The widespread growth of wireless technologies has made ambient exposure to radiofrequency electromagnetic fields (RF-EMF) ubiquitous. Previous studies have examined associations between mobile phone use and primary malignant brain tumor risk, yet the oncologic impact of ambient exposure remains unclear. Methods: We linked cellular infrastructure density from the OpenCelliD geodatabase to county-level brain tumor incidence in the National Cancer Institute’s Surveillance, Epidemiology, and End Results registry across 884 counties covering 46% of the U.S. population. Deployment followed a sigmoid growth pattern with an inflection in 2016; we compared infrastructure density and incidence ratios from 2011–2015 to 2016–2020, adjusting for baseline rates. Legacy cell tower infrastructure and LTE were examined separately, with vestibular schwannoma as a negative control, confounder adjustment, repeated-measures panels, and age stratification. Results: Growth in infrastructure density correlated with growth in total primary malignant brain tumors (r = 0.19, p = 2.2 × 10−8, 95% CI 0.122 to 0.250) and glioblastoma (r = 0.14, p = 5.5 × 10−5, 95% CI 0.070 to 0.200). The total-tumor association persisted after regressing out glioblastoma, though the non-GBM component attenuated to non-significance after full confounder adjustment. Vestibular schwannoma showed no significant association. The GBM association was significant for legacy cell tower infrastructure (r = 0.104, p = 0.0024, 95% CI 0.037 to 0.170) but non-significant for LTE, persisted after confounder adjustment, and was significant only in adults aged 70 and older. The GSM definition was post hoc, and its association was model-dependent. In the first-difference (repeated-measures) analysis, GBM was not significantly associated with legacy cell tower infrastructure (coefficient = 0.014, p = 0.70, 95% CI −0.060 to 0.088), while the association with all towers did not reach statistical significance (coefficient = 0.13, p = 0.052, 95% CI −0.001 to 0.251). Conclusions: County-level growth of cellular infrastructure is modestly associated with primary malignant brain tumor incidence. The legacy association was significant only in adults aged 70 and older; LTE and vestibular schwannoma showed no significant association. These findings are hypothesis-generating; causation is not established.

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