Ecological Analysis of Spatiotemporal Patterns in Brain Tumor Incidence and Cellular Infrastructure Growth in the United States
5 affiliations
- 1Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY 11549, USA
- 2The Feinstein Institutes for Medical Research, Manhasset, NY 11030, USA
- 3Department of Neurosurgery, Baylor College of Medicine, Houston, TX 77030, USA
- 4Northwell, New Hyde Park, NY 11042, USA
- 5Department of Neurosurgery, North Shore University Hospital, Manhasset, NY 11030, USA
Abstract
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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BibTeX
@article{barbero2026ecological,
title = {{Ecological Analysis of Spatiotemporal Patterns in Brain Tumor Incidence and Cellular Infrastructure Growth in the United States}},
author = {János A. Barbero and Prashin Unadkat and Daniel G. Eichberg and Randy S. D’Amico and Daniel M. Sciubba and Michael Schulder and Jung Park},
journal = {Cancers},
year = {2026},
month = oct,
doi = {10.3390/cancers18213419},
url = {https://www.mdpi.com/2072-6694/18/21/3419},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Ecological Analysis of Spatiotemporal Patterns in Brain Tumor Incidence and Cellular Infrastructure Growth in the United States
AU - János A. Barbero
AU - Prashin Unadkat
AU - Daniel G. Eichberg
AU - Randy S. D’Amico
AU - Daniel M. Sciubba
AU - Michael Schulder
AU - Jung Park
PY - 2026
DA - 2026/10/22
JO - Cancers
DO - 10.3390/cancers18213419
UR - https://www.mdpi.com/2072-6694/18/21/3419
AB - 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.
SN - 2072-6694
ER -