Radiofrequency at 2.45 GHz increases toxicity, pro-inflammatory and pre-apoptotic activity caused by black carbon in the RAW 264.7 macrophage cell line

The Science of the total environment · 2020 · Harm · Low evidence

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HarmLow evidencePaper 1880

RAW 264.7 macrophages exposed to 2.45 GHz RF in a GTEM chamber at sub-thermal SAR levels showed increased black carbon (BC)-induced toxicity, with effects observed at 24 h and remaining high at 72 h. Combined RF+BC exposure was associated with increased phago…

Study snapshot

PublicationThe Science of the total environment · 2020
Study typein_vitro
Reported directionHarm
Evidence ratingLow

Abstract

Radiofrequency at 2.45 GHz increases toxicity, pro-inflammatory and pre-apoptotic activity caused by black carbon in the RAW 264.7 macrophage cell line Rosa Ana Sueiro-Benavides, Jose Manuel Leiro-Vidal, Aarón Ángel Salas-Sánchez, J Antonio Rodríguez-González, Francisco J Ares-Pena, M Elena López-Martín. Radiofrequency at 2.45 GHz increases toxicity, pro-inflammatory and pre-apoptotic activity caused by black carbon in the RAW 264.7 macrophage cell line. Sci Total Environ. 2020 Oct 4;142681. doi: 10.1016/j.scitotenv.2020.142681. Abstract Environmental factors such as air pollution by particles and/or electromagnetic fields (EMFs) are studied as harmful agents for human health. We analyzed whether the combined action of EMF with fine and coarse black carbon (BC) particles induced cell damage and inflammatory response in RAW 264.7 cell line macrophages exposed to 2.45 GHz in a gigahertz transverse electromagnetic (GTEM) chamber at sub-thermal specific absorption rate (SAR) levels. Radiofrequency (RF) dramatically increased BC-induced toxicity at high doses in the first 24 h and toxicity levels remained high 72 h later for all doses. The increase in macrophage phagocytosis induced after 24 h of RF and the high nitrite levels obtained by stimulation with lipopolysaccharide (LPS) endotoxin 24 and 72 h after radiation exposure suggests a prolongation of the innate and inflammatory immune response. The increase of proinflammatory cytokines tumor necrosis factor-α, after 24 h, and of interleukin-1β and caspase-3, after 72 h, indicated activation of the pro-inflammatory response and the apoptosis pathways through the combined effect of radiation and BC. Our results indicate that the interaction of BC and RF modifies macrophage immune response, activates apoptosis, and accelerates cell toxicity, by which it can activate the induction of hypersensitivity reactions and autoimmune disorders. pubmed.ncbi.nlm.nih.gov

Machine Enhanced Logic

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 typein_vitro
Effect directionharm
PopulationRAW 264.7 macrophage cell line
Sample sizeNot supplied
ExposureRF · 2450 MHz · 24 h and 72 h
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

RAW 264.7 macrophages exposed to 2.45 GHz RF in a GTEM chamber at sub-thermal SAR levels showed increased black carbon (BC)-induced toxicity, with effects observed at 24 h and remaining high at 72 h. Combined RF+BC exposure was associated with increased phagocytosis (24 h), elevated nitrite levels after LPS stimulation (24 h and 72 h), increased TNF-α (24 h), and increased IL-1β and caspase-3 (72 h), consistent with enhanced pro-inflammatory and pro-apoptotic activity compared with BC alone.

Outcomes measured

  • Cell toxicity/viability
  • Inflammatory response
  • Macrophage phagocytosis
  • Nitrite levels (with LPS stimulation)
  • TNF-α
  • IL-1β
  • Caspase-3
  • Apoptosis pathway activation

Limitations

  • In vitro cell line model (RAW 264.7); findings may not generalize to humans
  • Specific absorption rate (SAR) value not reported in the abstract
  • Black carbon dosing details and exposure conditions not fully specified in the abstract
  • Sample size/replication not reported in the abstract
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 2450,
    "sar_wkg": null,
    "duration": "24 h and 72 h"
  },
  "population": "RAW 264.7 macrophage cell line",
  "sample_size": null,
  "outcomes": [
    "Cell toxicity/viability",
    "Inflammatory response",
    "Macrophage phagocytosis",
    "Nitrite levels (with LPS stimulation)",
    "TNF-α",
    "IL-1β",
    "Caspase-3",
    "Apoptosis pathway activation"
  ],
  "main_findings": "RAW 264.7 macrophages exposed to 2.45 GHz RF in a GTEM chamber at sub-thermal SAR levels showed increased black carbon (BC)-induced toxicity, with effects observed at 24 h and remaining high at 72 h. Combined RF+BC exposure was associated with increased phagocytosis (24 h), elevated nitrite levels after LPS stimulation (24 h and 72 h), increased TNF-α (24 h), and increased IL-1β and caspase-3 (72 h), consistent with enhanced pro-inflammatory and pro-apoptotic activity compared with BC alone.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro cell line model (RAW 264.7); findings may not generalize to humans",
    "Specific absorption rate (SAR) value not reported in the abstract",
    "Black carbon dosing details and exposure conditions not fully specified in the abstract",
    "Sample size/replication not reported in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "2.45 GHz",
    "radiofrequency",
    "RF",
    "GTEM chamber",
    "sub-thermal SAR",
    "black carbon",
    "RAW 264.7",
    "macrophage",
    "toxicity",
    "inflammation",
    "TNF-α",
    "IL-1β",
    "caspase-3",
    "apoptosis",
    "phagocytosis",
    "nitrite",
    "LPS"
  ],
  "suggested_hubs": [
    {
      "slug": "who-icnirp",
      "weight": 0.2,
      "reason": "Mentions sub-thermal SAR RF exposure; potentially relevant to exposure guideline discussions, though not explicitly policy-focused."
    }
  ]
}
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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.scitotenv.2020.142681
PubMed: 33071139

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