Non-Ionizing Radiation Created by Mobile Phone Progresses Endometrial Hyperplasia: An Experimental Rat Study

2019 · Harm · Low evidence

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HarmLow evidencePaper 1747

Study snapshot

Publicationmanual · 2019

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

Non-Ionizing Radiation Created by Mobile Phone Progresses Endometrial Hyperplasia: An Experimental Rat Study Fadiloglu E, Tapisiz OL, Unsal M, Fadiloglu S, Celik B, Mollamahmutoglu L. Non-Ionizing Radiation Created by Mobile Phone Progresses Endometrial Hyperplasia: An Experimental Rat Study. Arch Med Res. 2019 Feb;50(2):36-43. doi: 10.1016/j.arcmed.2019.05.010. Abstract BACKGROUND: Non-ionizing radiation is related with many pathologies. AIM: Determine association between non-ionizing radiation and endometrial hyperplasia. METHODS: Fifty oopherectomized Wistar albino rats were administered Estradiol hemihydrate (4 mg/kg) to induce hyperplasia, and were exposed to 1800 MHz radiation created by a mobile phone and a signal generator working as base station. This study was carried out with 5 groups in two phases. The study groups were. Control group without any exposure; group receiving estrogen in first phase of the study; group receiving estrogen in both phases; group receiving estrogen in the first phase and exposed to non-ionizing radiation during second phase and group taking estrogen in both phases and exposed to non-ionizing radiation during the second phase. Following both phases, uterine horns were excised and evaluated based on glandular density (GD), epithelial cell height (ECH), and luminal epithelial cell height (LECH). RESULTS: Estrogen increased all parameters during both phases (LECH, GD, and ECH values were 12,2 vs. 16,5 (p = 0.001), 34 vs. 47 (p <0.001), and 201 vs. 376.6 (p = 0.001), respectively during the first phase; LECH, GD and ECH values were 13,2 vs. 20,3 (p <0.001), 35.5 vs. 65,5 (p <0.001), 219.9 vs. 419.6 (p <0.001), respectively, during the second phase).Non-ionizing radiation increased all values without estrogen exposure (LECH, GD and ECH values were 13,2 vs. 17,2 (p = 0,074), 35,5 vs. 59 (p = 0.074), and 219 vs. 318.3 (p <0.001), respectively) or with estrogen exposure (LECH, GD, and ECH, values were 20,3 vs. 22,8 (p = 0,168), 65,5 vs. 77 (p = 0,058), and 419,6 vs. 541,6 (p = 0.004), respectively). CONCLUSION: Non-ionizing radiation progressed endometrial hyperplasia in an experimental rat model with/without estrogen exposure. ncbi.nlm.nih.gov

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typeanimal

Effect directionharm

PopulationOopherectomized Wistar albino rats administered estradiol hemihydrate to induce endometrial hyperplasia

Sample size50

ExposureRF · 1800 MHz

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

In this rat model, exposure to 1800 MHz non-ionizing radiation (mobile phone and signal generator acting as base station) increased LECH, GD, and ECH values compared with non-exposed groups, both without estrogen and with estrogen exposure; some comparisons were not statistically significant while ECH increases were statistically significant (p<0.001 without estrogen; p=0.004 with estrogen). The authors conclude that non-ionizing radiation progressed endometrial hyperplasia with/without estrogen exposure.

Outcomes measured

Endometrial hyperplasia-related histologic parameters: luminal epithelial cell height (LECH)
Glandular density (GD)
Epithelial cell height (ECH)

Limitations

Exposure duration and dosimetry (e.g., SAR) not reported in the abstract
Animal model; generalizability to humans not addressed in the abstract
Some reported increases did not reach statistical significance (e.g., LECH and GD comparisons with p values ~0.058–0.168 and 0.074)

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "mobile phone/base station (signal generator)",
    "frequency_mhz": 1800,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Oopherectomized Wistar albino rats administered estradiol hemihydrate to induce endometrial hyperplasia",
  "sample_size": 50,
  "outcomes": [
    "Endometrial hyperplasia-related histologic parameters: luminal epithelial cell height (LECH)",
    "Glandular density (GD)",
    "Epithelial cell height (ECH)"
  ],
  "main_findings": "In this rat model, exposure to 1800 MHz non-ionizing radiation (mobile phone and signal generator acting as base station) increased LECH, GD, and ECH values compared with non-exposed groups, both without estrogen and with estrogen exposure; some comparisons were not statistically significant while ECH increases were statistically significant (p<0.001 without estrogen; p=0.004 with estrogen). The authors conclude that non-ionizing radiation progressed endometrial hyperplasia with/without estrogen exposure.",
  "effect_direction": "harm",
  "limitations": [
    "Exposure duration and dosimetry (e.g., SAR) not reported in the abstract",
    "Animal model; generalizability to humans not addressed in the abstract",
    "Some reported increases did not reach statistical significance (e.g., LECH and GD comparisons with p values ~0.058–0.168 and 0.074)"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "non-ionizing radiation",
    "radiofrequency",
    "1800 MHz",
    "mobile phone",
    "base station",
    "endometrial hyperplasia",
    "estradiol",
    "rat",
    "Wistar",
    "oopherectomy"
  ],
  "suggested_hubs": [
    {
      "slug": "who-icnirp",
      "weight": 0.2,
      "reason": "RF exposure study relevant to broader RF health evidence base (no specific WHO/ICNIRP content stated)."
    }
  ]
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1016/j.arcmed.2019.05.010
PubMed: Not supplied

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