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 AnaSueiro-BenavidesaJose ManuelLeiro-VidalaAarón ÁngelSalas-SánchezbcJ. AntonioRodríguez-GonzálezbFrancisco J.Ares-PenabM. ElenaLópez-Martínd


•Black carbon and radiofrequency could be a suitable model for accelerated cellular toxicity.

•Electromagnetic fields and fine/coarse black carbon prolong innate and inflammatory immune responses.

•2.45 GHz radiofrequency and black carbon activate apoptosis of the RAW 264.7 macrophage cell line.


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.

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