Postnatal development & behavior effects of in-utero exposure of rats to RF emitted from WiFi devices

2017 · Mixed · Low evidence

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MixedLow evidencePaper 2284

Pregnant rats exposed to a 2.45 GHz WiFi signal for 2 h/day throughout gestation had offspring with impaired neurodevelopment during the first 17 postnatal days, while emotional and motor behavior at adult age was not altered. Prenatal WiFi exposure was assoc…

Study snapshot

Publicationmanual · 2017
Study typeanimal
Reported directionMixed
Evidence ratingLow

Abstract

Postnatal development & behavior effects of in-utero exposure of rats to RF emitted from WiFi devices Othman H, Ammari M, Rtibi K, Bensaid N, Sakly M, Abdelmelek H. Postnatal development and behavior effects of in-utero exposure of rats to radiofrequency waves emitted from conventional WiFi devices.Environ Toxicol Pharmacol. 2017 Apr 22;52:239-247. doi: 10.1016/j.etap.2017.04.016. Highlights • Effects of gestational exposure to 2.45 GHz WiFi signal for 2 h/day along gestation period on the offspring were studied. • Offspring showed neurodevelopment impairments but no behavior alteration at adult age. • Cerebral oxidative stress equilibrium as well as cholinesterase activity in brain and serum were altered. Abstract The present work investigated the effects of prenatal exposure to radiofrequency waves of conventional WiFi devices on postnatal development and behavior of rat offspring. Ten Wistar albino pregnant rats were randomly assigned to two groups (n=5). The experimental group was exposed to a 2.45GHz WiFi signal for 2h a day throughout gestation period. Control females were subjected to the same conditions as treated group without applying WiFi radiations. After delivery, the offspring was tested for physical and neurodevelopment during its 17 postnatal days (PND), then for anxiety (PND 28) and motricity (PND 40-43), as well as for cerebral oxidative stress response and cholinesterase activity in brain and serum (PND 28 and 43). Our main results showed that the in-utero WiFi exposure impaired offspring neurodevelopment during the first seventeen postnatal days without altering emotional and motor behavior at adult age. Besides, prenatal WiFi exposure induced cerebral oxidative stress imbalance (increase in malondialdehyde level (MDA) and hydrogen peroxide (H2O2) levels and decrease in catalase (CAT) and superoxide dismutase (SOD) activities) at 28 but not 43days old, also the exposure affected acethylcolinesterase activity at both cerebral and seric levels. Thus, the current study revealed that maternal exposure to WiFi radiofrequencies led to various adverse neurological effects in the offspring by affecting neurodevelopment, cerebral stress equilibrium and cholinesterase activity. 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 directionmixed
PopulationPregnant Wistar albino rats and their offspring
Sample size10
ExposureRF · 2450 MHz · 2 h/day throughout gestation
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Pregnant rats exposed to a 2.45 GHz WiFi signal for 2 h/day throughout gestation had offspring with impaired neurodevelopment during the first 17 postnatal days, while emotional and motor behavior at adult age was not altered. Prenatal WiFi exposure was associated with cerebral oxidative stress imbalance at PND 28 (but not PND 43) and altered acetylcholinesterase activity in brain and serum.

Outcomes measured

  • Physical development (postnatal days 1–17)
  • Neurodevelopment (postnatal days 1–17)
  • Anxiety (PND 28)
  • Motricity/motor behavior (PND 40–43)
  • Cerebral oxidative stress markers (MDA, H2O2, CAT, SOD) (PND 28 and 43)
  • Cholinesterase (acetylcholinesterase) activity in brain and serum (PND 28 and 43)

Limitations

  • Small sample size (10 pregnant rats; n=5 per group)
  • SAR/dosimetry not reported in abstract
  • Animal study; generalizability to humans not addressed in abstract
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "wi-fi",
    "frequency_mhz": 2450,
    "sar_wkg": null,
    "duration": "2 h/day throughout gestation"
  },
  "population": "Pregnant Wistar albino rats and their offspring",
  "sample_size": 10,
  "outcomes": [
    "Physical development (postnatal days 1–17)",
    "Neurodevelopment (postnatal days 1–17)",
    "Anxiety (PND 28)",
    "Motricity/motor behavior (PND 40–43)",
    "Cerebral oxidative stress markers (MDA, H2O2, CAT, SOD) (PND 28 and 43)",
    "Cholinesterase (acetylcholinesterase) activity in brain and serum (PND 28 and 43)"
  ],
  "main_findings": "Pregnant rats exposed to a 2.45 GHz WiFi signal for 2 h/day throughout gestation had offspring with impaired neurodevelopment during the first 17 postnatal days, while emotional and motor behavior at adult age was not altered. Prenatal WiFi exposure was associated with cerebral oxidative stress imbalance at PND 28 (but not PND 43) and altered acetylcholinesterase activity in brain and serum.",
  "effect_direction": "mixed",
  "limitations": [
    "Small sample size (10 pregnant rats; n=5 per group)",
    "SAR/dosimetry not reported in abstract",
    "Animal study; generalizability to humans not addressed in abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "prenatal exposure",
    "gestational exposure",
    "WiFi",
    "2.45 GHz",
    "radiofrequency",
    "rat offspring",
    "neurodevelopment",
    "oxidative stress",
    "malondialdehyde",
    "hydrogen peroxide",
    "catalase",
    "superoxide dismutase",
    "acetylcholinesterase",
    "behavior"
  ],
  "suggested_hubs": [
    {
      "slug": "school-wi-fi",
      "weight": 0.55,
      "reason": "Exposure source is conventional WiFi devices (2.45 GHz)."
    }
  ]
}
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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.etap.2017.04.016
PubMed: Not supplied

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