# RF-028 — Delayed albumin leakage, with a specific significant exposure comparison

Why this matters
Researchers detected a blood protein outside brain vessels a week after exposure, suggesting altered control of passage into brain tissue. They did not find an increase in dark-staining nerve cells. The question is whether the reported barrier change is reproducible and has consequences for brain function.

Id: RF-028

Author: Nittby et al.

Full Authors: Henrietta Nittby; Arne Brun; Jacob Eberhardt; Lars Malmgren; Bertil R. R. Persson; Leif G. Salford

Year: 2009

Title: Increased blood-brain barrier permeability in mammalian brain 7 days after exposure to the radiation from a GSM-900 mobile phone

Journal: Pathophysiology

Citation: Nittby H, Brun A, Eberhardt J, Malmgren L, Persson BRR, Salford LG. Increased blood-brain barrier permeability in mammalian brain 7 days after exposure to the radiation from a GSM-900 mobile phone. Pathophysiology. 2009;16(2-3):103-112. doi:10.1016/j.pathophys.2009.01.001.

Doi: 10.1016/j.pathophys.2009.01.001

Pmid: 19345073

Topic: Neuropathology and blood-brain barrier

Verification Group: Original text reviewed

Record Role: Original text reviewed

Featured: False

Exposure: GSM-900; 2 h in TEM cells; whole-body SAR sham, 0.12, 1.2, 12, 120 mW/kg; 7-day recovery.

Design: 48 male/female Fischer 344 rats aged 2-3 months: 8/group at four active levels, 16 sham. Awake, movable; 7-day recovery; perfusion fixation, albumin immunohistochemistry/cresyl-violet; pathologist blinded; ordinal scoring. Brain-SAR orientation variability 56% standard deviation around mean.

Finding: At 7 days, focal albumin leakage occurred in 25% of exposed versus 0% sham rats (Fisher exact p=0.04); five-group score comparison p=0.012. The 12 mW/kg comparison was significant (p=0.007); 0.12 and 120 mW/kg were trends (p=0.1). Neuronal albumin uptake differed globally (p=0.03) and at 1.2 mW/kg versus sham (p=0.02). Dark-neuron occurrence did not differ.

Boundary: Original article-in-press proof reviewed. These are BBB/albumin endpoints, without increased dark-neuron pathology at 7 days. Trends are not significant findings. No claim of human-limit compliance from rat whole-body SAR.

Related: Same Lund research programme as RF-020 and RF-027; separate 7-day experiment, not the 14/28-day animals.

Protection Question: Is the delayed barrier change reproducible, and does it affect brain function? Passage of a blood protein into tissue is distinct from neuronal injury; dark neurons did not increase here.

Access: Original 10-page article-in-press proof hosted by California Council on Science and Technology; methods, results and funding reviewed

Locator: Proof pp.5-7 sections 3.1-3.4 and 4; p.8 Acknowledgements; final pp.103-112

Notice: Scite metadata checked 20 Oct 2026; no editorial notice returned. Primary bibliographic records and targeted notices were checked where retrievable; no retraction or expression of concern located. This is not certification that no notice exists.

Funding: Hans and Märit Rausing Charitable Foundation (proof p.8).

Conflicts: No competing-interest declaration located in original proof; no inference.

Source Url: https://doi.org/10.1016/j.pathophys.2009.01.001

Retrieval Links: https://doi.org/10.1016/j.pathophys.2009.01.001 | https://lup.lub.lu.se/record/1392465 | https://pubmed.ncbi.nlm.nih.gov/19345073/ | https://ccst.us/wp-content/uploads/082009_Nittby_Increased_Permeability.pdf

Verification Date: 2026-10-20

